Name: ___________________________ Class: _________________ Date: __________
Chapter 01 1. The last cases of smallpox were reported in the a. 1950s. b. 1960s. c. 1970s. d. 1980s. e. 1990s.
2. The first line of defense against microorganisms that infect the body is referred to as __________ immunity. a. opportunistic b. innate c. adaptive d. primary e. central
3. Select the correct statement about innate and adaptive immunity. a. Innate immunity involves cells bearing receptors that are highly specific for a pathogen. b. The first response to a pathogen involves immunological memory. c. Hematopoiesis occurs in the lymph node. d. Phagocytosis involves the uptake and killing of microbes. e. Once lymphocytes mature, they remain in lymphoid organs and do not reenter the blood.
4. Which of the following are chemical barriers of innate immunity? a. lactic acid and lysozyme b. lactic acid, lysozyme, and the normal microbiota c. skin and mucous membranes
d. neutrophils and macrophages e. All of these answers are correct.
5. When macrophages secrete __________, an inflammatory response ensues. a. lysozyme b. defensins c. lymph d. sebum e. cytokines
6. The thin layer of cells that makes up the interior lining of the blood vessels is called the a. mucosa. b. epithelium. c. endothelium. d. connective tissue. e. lymphoid tissue.
7. Identify the incorrect statement regarding hematopoiesis. a. Hematopoiesis is a continuous process that occurs throughout one’s lifetime. b. The location for hematopoiesis differs with age. c. Self-renewal is necessary to replenish the supply of hematopoietic stem cells. d. Most hematopoiesis occurs in the bone marrow after birth. e. Leukocytes, but not erythrocytes, must go through hematopoiesis to develop.
8. The progenitors of macrophages are a. megakaryocytes. b. dendritic cells. c. monocytes. d. neutrophils.
e. M cells.
9. __________ act as cellular messengers by delivering degraded pathogens to lymphoid organs. a. Plasma cells b. Dendritic cells c. Large granular lymphocytes d. Mast cells e. Basophils
10.Another name for a large granular lymphocyte is a a. plasma cell. b. helper T cell. c. monocyte. d. natural killer cell. e. eosinophil.
11.Effector cells that secrete antibodies are known as __________ cells. a. natural killer b. cytotoxic T c. helper T d. M e. plasma
12.Spherical regions in lymph nodes containing areas that are packed densely with proliferating B cells are called a. efferent vessels. b. germinal centers. c. red pulp zones. d. periarterial lymphoid sheaths. e. medullary sinuses.
13.The __________ is/are the lymphoid organ(s) that filter(s) the blood. a. spleen b. tonsils c. Peyer’s patches d. appendix e. adenoids
14.__________ cells persist long after an individual has been vaccinated. a. Neutrophil b. Plasma c. Memory d. M e. Mast
15.During an infection, __________ are mobilized in large numbers from the bone marrow. a. dendritic cells b. memory cells c. macrophages d. neutrophils e. B cells
16.In most cases, the adaptive immune response relies on the initial activation of CD4 T cells by the antigen-presenting __________ that have entered a secondary lymphoid tissue through the afferent lymph. a. macrophages b. CD8 T cells c. B cells d. dendritic cells e. epithelium
17.Select the statement that is characteristic of a secondary immune response.
a. Secondary immune responses are activated when primary immune responses fail to completely eradicate an infection. b. Secondary immune responses occur in both innate and adaptive immune responses. c. Memory cells are activated rapidly during a secondary immune response. d. Secondary immune responses are orders of magnitude smaller than primary immune responses. e. All of these answers are correct.
18.A bacterium that causes a common disease in a population that has been previously exposed to it is called a. opportunistic. b. resistant. c. commensal. d. endemic. e. attenuated.
19.An example of an antimicrobial substance that protects epithelial surfaces from pathogens by degrading the bacterial cell wall is a. glycoprotein. b. complement. c. proteoglycan. d. lysozyme. e. sebum.
20.Which of the following is characteristic of innate immunity? a. inflammation b. improvement in recognition of the pathogen during the response c. slow response d. highly specific for a particular pathogen e. All of these answers are correct.
21.Which statement about neutrophils is NOT true?
a. Neutrophils are mobilized from the bone marrow to sites of infection when needed. b. Neutrophils are active only in aerobic conditions. c. Neutrophils are phagocytic. d. Neutrophils form pus, which comprises dead neutrophils. e. Dead neutrophils are cleared from sites of infection by macrophages.
22.Primary lymphoid tissues are the sites where lymphocytes __________, whereas secondary lymphoid tissues are the sites where lymphocytes __________. a. are stimulated; develop and mature b. encounter pathogens; undergo apoptosis c. develop and mature; become stimulated d. undergo clonal selection; differentiate from hematopoietic stem cells e. die; are phagocytosed after death.
23.The spleen differs from other secondary lymphoid organs in which of the following ways? a. It does not contain T cells. b. It filters blood as well as lymph. c. It is populated by specialized cells called M cells. d. It receives pathogens via afferent lymphatic vessels. e. It has no connection with the lymphatics.
24.Examples of pathogens that cause human disease include a. bacteria. b. viruses. c. fungi. d. parasites (protozoans and worms). e. All of these are examples of pathogens that cause human disease.
25.Which of the following is NOT associated with mucosal surfaces? a. mucus-secreting goblet cells
b. lysozyme c. M cells d. white pulp e. beating cilia
26.A term generally used to describe all white blood cells is __________. a. hematopoietic cells b. myeloid progenitor c. dendritic cells d. monocytes e. leukocytes
27.The most abundant type of leukocyte in human peripheral blood is the a. eosinophil. b. basophil. c. neutrophil. d. monocyte. e. lymphocyte.
28.Which of the following statements is correct? a. Macrophages are granulocytes. b. Macrophages derive from neutrophils. c. Macrophages are non-phagocytic. d. Macrophages reside in the tissues. e. All of these statements are false.
29.Select the correct statement about hematopoiesis. a. During human development, hematopoiesis takes place at different anatomical locations. b. The hematopoietic stem cell gives rise to white blood cells, but a different stem cell is the progenitor of red blood cells. c. Hematopoietic stem cells are able to differentiate but not divide.
d. Platelets differentiate from red blood cells. e. Megakaryocytes are small cells lacking a nucleus.
30.Which of the following describes the flow of lymph through a lymph node draining an infected tissue? a. efferent lymphatic vessel > lymph node > afferent lymphatic vessel b. venule > lymph node > efferent lymphatic vessel c. afferent lymphatic vessel > lymph node > efferent lymphatic vessel d. artery > lymph node > efferent lymphatic vessel e. afferent lymphatic vessel > lymph node > artery
31.Immune cells within the lymphatic circulation are directly deposited into which of the following anatomical sites so that the cells may reenter the bloodstream? a. right aorta b. left subclavian vein c. left carotid artery d. high endothelial venule e. hepatic vein
32.Which of the following is the predominant route by which pathogens are brought from a site of infection into a lymph node? a. efferent lymphatics b. artery c. vein d. afferent lymphatics e. high endothelial venule
33.Vaccination is best described as prevention of severe disease by a. the deliberate introduction of a virulent strain of an infectious agent. b. prior exposure to an infectious agent in a related, but weakened form. c. prophylactic treatment with antibiotics. d. stimulating effective innate immune responses.
e. using effective public-health isolation regimens such as quarantine.
34.Which statement explains why immunity to influenza may appear to be relatively short-lived? a. Effective immunological memory fails to develop. b. Immune responses to influenza involve innate immune mechanisms only. c. The primary and secondary immune responses are equivalent. d. Influenza virus targets memory cells. e. New influenza variants able to escape previous immunity appear regularly.
35.Select the correct statement concerning the gut-associated lymphoid tissue.
a. Number 1 refers to the cell that transports antigen from the lumen across the mucosa. b. Number 2 highlights the B cell–rich region of the gut-associated lymphoid tissue. c. Number 3 identifies the afferent lymphatics. d. Number 4 identifies the germinal center, which is the site of resting B cells that have not yet been activated by antigen. e. All of these answers are correct.
36.Select the correct statement concerning the gut-associated lymphoid tissue (GALT). a. Antigen enters the GALT via the afferent lymphatic vessels.
b. T cells do not recirculate to the GALT. c. Tonsils, Peyer’s patches, and the appendix are all part of the GALT. d. The GALT is a primary lymphoid tissue. e. All of these answers are correct.
37.Which of the following would likely occur during an effective immune response to the SARS-CoV-2 virus? a. MHC class I would present SARS-CoV-2 viral peptides. b. Epitopes located on the SARS-CoV-2 surface would be bound by antibodies. c. A neutralizing antibody response would be generated. d. B cells would undergo clonal selection and clonal expansion. e. All of the these answers are correct.
38.State the location where monocytes and neutrophils develop in adults.
39.Compare how B and T cells recognize antigen.
40.Why does it take approximately a week after infection for the benefits of an adaptive immune response to start to be felt?
41.Compare granulocytes to monocytes, including physical features and their functions.
42.Identify the different anatomical locations where hematopoiesis occurs in embryonic, fetal, and adult life.
43.What are clonal selection and clonal expansion in the context of an adaptive immune response? Describe how they shape the adaptive immune response.
44.What would be the consequence of a bioterrorist attack that released smallpox virus into a city?
45.Phagocytosis of either microbes or microbial constituents by macrophages is followed by the activation of macrophages and the secretion of cytokines. What are the main effects of these cytokines?
46.Identify the four classes of pathogens that provoke immune responses in our bodies and give an example of each.
47.Identify the two major progenitor subsets of leukocytes and the types of cells that differentiate from each progenitor.
48.How can antibiotics upset the barrier function of intestinal epithelia? Give a specific example.
49.Describe the characteristics commonly associated with inflammation and what causes them.
50.Describe the three main ways in which epithelia function as a barrier to infection, giving details of the mechanisms employed and the sites of the body protected.
51.Describe three distinct mechanisms by which antibodies eradicate infection.
52.What are the main differences between innate immunity and adaptive immunity?
Answer Key Chapter 01 1. Answer: C 2. Answer: B 3. Answer: D 4. Answer: A 5. Answer: E 6. Answer: C 7. Answer: E 8. Answer: C 9. Answer: B 10.Answer: D 11.Answer: E 12.Answer: B 13.Answer: A 14.Answer: C 15.Answer: D 16.Answer: D 17.Answer: C 18.Answer: D 19.Answer: D 20.Answer: A
21.Answer: B 22.Answer: C 23.Answer: E 24.Answer: E 25.Answer: D 26.Answer: E 27.Answer: C 28.Answer: D 29.Answer: A 30.Answer: C 31.Answer: B 32.Answer: D 33.Answer: B 34.Answer: E 35.Answer: A 36.Answer: C 37.Answer: E 38.Answer: In adults, all leukocytes originate in the bone marrow and are derived from pluripotent hematopoietic stem cells. 39.Answer: Both B and T cells have antigen receptors with variable regions that bind with
high specificity to a region of the antigen. The antigen-binding site of immunoglobulin is made up of the tips of two variable regions, whereas the T-cell receptor has one antigen-binding site. The B-cell receptor can recognize carbohydrates, glycoproteins, proteoglycans, and glycolipids on the surface of microbial pathogens. B-cell receptors and antibodies recognize the native conformation, or three-dimensional structure, of the antigen. In contrast, the epitope recognized by a T-cell receptor is a short peptide of 8–16 amino acids in length that is presented by an MHC molecule on the surface of another cell. 40.Answer: Before the establishment of an effector population of lymphocytes, several events must occur: (1) specific recognition of pathogen by lymphocyte receptors (clonal selection); (2) proliferation of pathogen-specific lymphocytes to expand responding populations (clonal expansion); and (3)
differentiation into effector lymphocytes with the resulting establishment of an organized adaptive immune response. 41.Answer: The granulocytes are defined by prominent granules containing molecules that kill microbes and enhance inflammation and irregularly shaped nuclei. The granulocytes include neutrophils, basophils, and eosinophils. Neutrophils are phagocytic cells; eosinophils provide protection against helminth worms; and basophils initiate the anti-parasite response and function as regulatory cells. In comparison, monocytes are larger than granulocytes and have a more uniform appearance including a distinctive indented nucleus. Monocytes circulate in the blood and are recruited to tissues where they differentiate into macrophages. Monocytes and macrophages are both phagocytic. 42.Answer: The yolk sac and the liver produce blood cells in the embryo and early fetus through the first three months of gestation.
The fetal spleen takes over this function from the third to the seventh months. Once developed, the bone marrow is the site of hematopoiesis from the fourth month of gestation throughout the remainder of fetal development and into adulthood. 43.Answer: In an adaptive immune response to a pathogen, the term clonal selection describes the fact that only those lymphocytes that can recognize that particular pathogen and respond to it are selected to participate in the immune response. Clonal expansion describes the proliferation and subsequent differentiation of these few original lymphocytes to provide large numbers of effector lymphocytes. Clonal selection ensures that the adaptive response will be tailored specifically for the particular type of pathogen involved in the infection. Clonal expansion ensures that the few original lymphocytes specific for the pathogen produce a large population of effector lymphocytes that can make an effective
immune response against the pathogen. 44.Answer: The last case of smallpox was reported in the 1970s. As a result, children are no longer vaccinated routinely as was the case before smallpox was eradicated. A large proportion of any given population today would be unvaccinated, and thus susceptible to smallpox infection. The mortality rate would be high (30–50 percent) among those not protected by vaccination. 45.Answer: The cytokines released by activated macrophages have three principal effects. Some cytokines act as chemoattractants and recruit other leukocytes into the infected tissue, for example, neutrophils, which efficiently phagocytose and kill bacteria, forming pus. Cytokines increase the adhesive properties of the blood endothelium, allowing cells such as neutrophils to adhere and leave the blood to enter tissues. Other cytokines act on the endothelial cells of local blood vessels to increase vascular permeability and
vasodilation, thus initiating inflammation of the infected tissue. 46.Answer: The four classes of pathogens are bacteria, viruses, fungi, and parasites (protozoa and worms). 47.Answer: The two major progenitor subsets of leukocytes are the common lymphoid progenitor and the myeloid progenitor. The common lymphoid progenitor differentiates into three cell types: B cells, T cells, and natural killer (NK) cells. The myeloid progenitor differentiates into six main cell types: basophils, eosinophils, neutrophils, mast cells, dendritic cells, and monocytes. Monocytes are circulating leukocytes that enter tissues, where they then differentiate into macrophages. 48.Answer: Antibiotics attack the microbiological barriers of intestinal epithelia. The normal microbiota sensitive to the antibiotics are killed off, and the intestine can then be recolonized and overgrown by microorganisms that in normal circumstances
are present in very small numbers and thus do not cause a problem. An example is a condition called pseudomembranous colitis caused by the overgrowth of Clostridium difficile. The toxin produced by Clostridium leads to diarrhea and bleeding, and may cause death, particularly in elderly patients. 49.Answer: The hallmarks of inflammation are heat, redness, pain, and swelling (edema). These are caused by a combination of vasodilation (causing redness and heat), increased vascular permeability, and the consequent infiltration of fluid and leukocytes from the blood into the infected site (causing swelling and pain as a result of the increased pressure on local nerve endings). 50.Answer: (1) Mechanical (physical) barriers. The tough outer barrier of layers of keratinized cells on the skin help make it impenetrable. On ciliated epithelial surfaces, such as those of the respiratory tract, the formation of a layer of mucus that is kept in continual movement
by the beating cilia inhibits colonization and invasion by microorganisms. (2) Chemical barriers. The epithelium produces a variety of chemical substances that interfere with the adherence of microorganisms to epithelium and their replication. The skin produces fatty acids in sebaceous glands, which helps to create an acid environment inhibitory to the growth of many bacteria. Lysozyme, an enzyme that inhibits cell-wall formation in bacteria, is secreted in tears, saliva, and sweat. The acidic environments of the stomach, vagina, and skin prevent microbial growth. (3) Microbiological barriers. A microbiota of non-pathogenic commensal microorganisms colonizes many epithelial surfaces and provides an additional barrier to infection. They compete with pathogenic microbes for space and nutrients, and sometimes produce antibacterial proteins that further inhibit attachment to epithelium. For example, Escherichia coli in the large intestine produce colicins, which prevent
colonization by other bacteria. The sites protected are the skin, mucosal epithelium of the gastrointestinal tract, mucosal epithelium of the respiratory tract, and the mucosal epithelium of the urinogenital tract. 51.Answer: (1) Neutralization. By binding to the surface of a pathogen, antibodies interfere with the ability of the pathogen to grow and replicate. Antibody binding to a pathogen or a bacterial toxin can also inhibit its binding to receptors on host cells and therefore prevent its entry into cells. (2) Opsonization. Antibody coating the surface of a pathogen or toxin can promote phagocytosis of the antibody-covered particle. Antibodies acting in this way are known as opsonins. The antibody-bound material interacts with Fc receptors on the surface of phagocytic cells such as macrophages and neutrophils, which bind the constant region (the stem) of the antibody. Stimulation of Fc receptors in this way stimulates the engulfment and degradation of antibody-coated
material by the phagocyte. (3) Complement activation. IgG or IgM antibody bound to a pathogen stimulates activation of the complement system, leading to the deposition of complement proteins on the surface of the pathogen. Certain of these act as opsonins and bind to complement receptors on phagocytic cells to stimulate the phagocytosis and destruction of the pathogen. 52.Answer: Innate immune responses are initiated almost immediately after infection, whereas adaptive immunity takes longer to develop. Innate immunity uses generalized and invariant mechanisms to recognize pathogens. Examples of these are the receptors on phagocytes that recognize surface molecules shared by many different pathogens and stimulate phagocytosis, and serum proteins such as complement. Innate immunity is often unable to eradicate the pathogen completely, and even when it does, it does not
produce immunity to reinfection. An adaptive immune response, in contrast, involves specific recognition of the particular pathogen by highly specific receptor on a subset of lymphocytes, which are selected from a pool of millions of lymphocytes each bearing receptors specific for different molecules. Adaptive immunity is often powerful enough to eradicate the infection and provides longterm protective immunity through immunological memory.
Name: ___________________________ Class: _________________ Date: __________
Chapter 02 1. Soluble effector molecules a. are effective when encountering pathogens in both extracellular spaces and the cytosol. b. are not effective against viruses at any stage of infection. c. often provide protection during the late stages of the immune response. d. include the pentraxins. e. All of these answers are correct.
2. Which of the three complement pathways becomes activated soonest after an initial infection? a. the classical pathway b. the lectin pathway c. the alternative pathway
3. All of the following complement proteins help form a pore in the pathogen’s membrane except a. C3b. b. C5b. c. C6. d. C7. e. C8. f. C9.
4. The importance of CD59 (also known as protectin) is to a. promote the speed of complement activation by protecting C3 convertase C3bBb from proteolytic degradation. b. prevent the recruitment of C9. c. dissociate the components of the alternative C3 convertase. d. prevent the attachment of C3b to host cell surfaces.
e. inhibit the anchoring of C5b, C6, and C7 to host cell surfaces.
5. __________ are soluble complement fragments that mediate localized and systemic inflammatory responses. a. cryptdins b. defensins c. anaphylatoxins d. selectins e. c-reactive proteins
6. Alpha2-macroglobulin a. binds covalently to its target via a disulfide bond. b. is not found in the circulation until several hours after microbial infection. c. possesses protease activity to cleave microbial targets. d. binds its target and is cleared from the circulation by cells bearing receptors specific for the complex. e. targets the membrane-attack complex on human cells.
7. Which of the following is the soluble form of C3 convertase of the alternative pathway of complement activation? a. iC3 b. iC3b c. C3b d. iC3Bb e. C3bBb
8. Which of the following does not accurately describe complement components? a. soluble proteins b. made by the spleen c. located in extracellular spaces d. some function as proteases once activated e. activated by a cascade of enzymatic reactions
9. Which of the following is the membrane-bound form of C3 convertase of the alternative pathway of complement activation? a. iC3 b. C3a c. C3b d. iC3Bb e. C3bBb
10.The plasma proteins that counteract the activity of factor P by inactivating C3 convertase through the cleavage of C3b are a. factor B and factor H. b. factor H and factor I. c. factor B and factor I. d. decay-accelerating factor and factor H. e. decay-accelerating factor and membrane cofactor protein.
11.The membrane-bound proteins on human cells that dissociate and inactivate alternative C3 convertase to avoid complement activation are a. factor B and factor H. b. factor H and factor I. c. factor B and factor I. d. decay-accelerating factor and factor H. e. decay-accelerating factor and membrane cofactor protein.
12.Which of the following complement components is an opsonin that binds to complement receptor 1 (CR1) on macrophages? a. C3b b. C3a c. Bb d. Ba e. C3bBb.
13.Which of the following polymerizes to form a transmembrane channel that compromises the integrity of cell membranes? a. C5 b. C6 c. C7 d. C8 e. C9
14.Which of the following are important in anchoring the membrane-attack complex to the membrane? a. C3 and C5 b. C5 and C6 c. C6 and C7 d. C7 and C8 e. C8 and C9
15.In an individual lacking the enzyme to produce a glycosylphosphatidylinositol (GPI) lipid tail, which of the following proteins will still be expressed normally? a. decay-accelerating factor (DAF) b. homologous restriction factor (HRF) c. membrane cofactor protein (MCP) d. protectin (CD59) e. None of these answers are correct.
16.The ligand for CR3 and CR4 formed by the cleavage of C3b by the combined action of factors H and I is called a. C3bBb. b. C3a. c. C3b2Bb. d. iC3b. e. C5b.
17.Which of the following does not describe the actions of the coagulation system? a. blood clot formation b. enhancement of dissemination of microbes into lymphatics and bloodstream c. decrease in blood loss and fluid into interstitial spaces in tissues d. release of inflammatory mediators by platelets e. wound healing
18.Damage to tissues triggers a cascade of plasma proteins involving bradykinin and is known as a. the alternative pathway of complement. b. the coagulation system. c. the kinin system. d. receptor-mediated endocytosis. e. the acute-phase response.
19.Which of the following does not accurately describe the defensins? a. They are highly conserved with few variants. b. They contain a large proportion of arginine residues. c. They contain three intra-chain disulfide bonds. d. They are amphipathic, with hydrophobic and hydrophilic regions. e. They disrupt pathogen membranes by penetrating them and disrupting their integrity.
20.The microbiota a. triggers the immune system to stop developing after birth. b. refers to pathogenic bacteria that invade during infection. c. competes with pathogens for nutrients. d. is composed of ten key bacterial species. e. is absent in germ-free mice.
21.Select the correct response concerning the three lines of immune defense.
a. Low pH in the stomach and the antimicrobial enzymes of tears are part of the induced innate immune response. b. Factors that increase in activity or concentration following pathogen detection are part of the induced innate immune response. c. The adaptive immune response peaks within the first 96 hours of infection. d. All of these answers are correct. e. None of these answers are correct.
22.Which of the following provide immune defense against viruses in the extracellular phase? a. pentraxins b. defensins c. complement d. All of these answers are correct. e. None of these answers are correct.
23.Select the correct statement about complement and macrophages.
a. The bacterial cell is opsonized by C3a, which is bound by CR1 leading to endocytosis by the macrophage. b. The bacterial cell is opsonized by C3bBb, which is bound by CR1 leading to endocytosis by the macrophage. c. Opsonization is due to the formation of a covalent bond between the microbial surface and CR1. d. Opsonization is prevented by the activity of decay accelerating factor. e. Opsonization occurs in the alternative pathway of complement activation, but not in the classical pathway.
24.Clostridium difficile
a. is a commensal organism that benefits its human host. b. outcompetes resident commensals to cause illness following antibiotic treatment. c. is an example of a viral infection. d. is part of the microbiological barrier protecting us from infection.
25.Extracellular pathogens a. replicate within the host cell. b. are cleared when the host cell is killed. c. are targets of soluble molecules such as complement or antibodies. d. are found only on the skin. e. None of these answers are correct.
26.In the complement pathway, regulatory proteins a. decrease complement activity by stabilizing membrane-bound C3b. b. decrease complement activity by preventing C3b degradation by proteases. c. decrease complement activity by disrupting the alternative C3b convertase. d. increase complement activity by allowing C3b to be fixed on the surface of human cells. e. increase complement activity by preventing C3bBb degradation by proteases.
27.Pentraxins a. circulate in the blood, but not in the lymph. b. are classified as part of the adaptive immune response. c. function to generate the alternative C3 convertase. d. simultaneously bind pathogens and receptors on phagocytes. e. are made only by the liver cells.
28.Select the correct statement concerning defensins. a. Each bacterial toxin requires one unique defensin protein to inactivate it. b. Defensins are similar to chaperone proteins as they aid proper folding and function of other proteins.
c. Bacterial toxins are thermodynamically stable and structurally rigid, enabling their inactivation by defensins. d. Defensins are large proteins composed of three subunits. e. Human proteases aid the defensins in inactivating bacterial toxins.
29.Select the statement that is accurate concerning plasma proteins. a. The key function of the coagulation system is to promote blood vessel dilation leading to elimination of pathogens and repair of tissues. b. Platelets release factors that recruit immune-system cells and lead to tissue repair. c. The coagulation and kinin systems both lead to the production of blood clots. d. The α2-macroglobulin proteins activate the classical complement pathway, thus helping to clear pathogens.
30.Which of the following best describes the innate immune system? a. Epithelial tight junctions are considered a chemical barrier. b. The mechanical barrier of the skin likely acts to prevent infection before induced innate mechanisms of immunity. c. Complement proteins are not present prior to infection and must be produced following infection with a pathogen. d. Following a first exposure to a pathogen, an individual does not need the innate immune system if they produce a strong adaptive response within 24 hours.
31.Although activation of the three different pathways of complement involves different components, the three pathways converge on a common enzymatic reaction referred to as complement fixation. Describe this reaction.
32.Compare the C3 convertase generated by the three different pathways of complement.
33.Explain the steps that take place when a bacterium is opsonized via C3b:CR1
interaction between the bacterium and a resident macrophage in tissues.
34.In the early stages of the alternative pathway of complement activation there are complement control proteins that are both soluble (factors H and I) and associated with the cell surface (DAF and MCP). Identify the (i) soluble and (ii) cell surface–associated complement control proteins that operate in the terminal stages of the alternative pathway of complement activation, and describe their activities.
35.Why is it important to expose the hydrophobic sites of C7 and C8 during the formation of the membrane-attack complex?
36.Explain the similarities between membrane cofactor protein and factor H in terms of their complement control properties.
37.Identify proteins A, B, and C of the complement pathway.
38.Identify the three effector mechanisms of complement that help clear a microbial infection.
5. This figure shows the interaction of natural killer cells with activated macrophages. Is the following statement true or false? NK cells exit the bone marrow unable to undergo further proliferation. a. True b. False
6. This figure shows the interaction of natural killer cells with activated macrophages. Is the following statement true or false? Both the NK cell and the macrophage express receptors for IL-15. a. True b. False
7. C-type lectins are so called because of the role of __________ in facilitating receptor–ligand interactions.
a. carbohydrate b. CR1 c. calcium d. chemokines e. caspases
8. Lectins recognize microbial a. phosphate-containing lipoteichoic acids. b. nucleic acids. c. carbohydrates. d. flagellin. e. sulfated polysaccharides.
9. Scavenger receptors do not recognize a. lipopolysaccharides. b. lipoteichoic acid. c. phosphatidyl serine. d. CpG-rich bacterial DNA. e. mannose.
10.Macrophages bear on their surface receptors for all of the following EXCEPT a. mannose. b. glucans. c. C3b. d. lipopolysaccharide. e. CpG-rich bacterial DNA.
11.__________ is a soluble protein. a. TLR4 b. CD14 c. lipopolysaccharide-binding protein (LBP) d. CXCR1
e. MARCO
12.__________ belong to a family of structurally similar membrane-bound proteins that aid in the adhesion between various types of human cell. a. Interferons b. Integrins c. GTP-binding proteins d. Pyrogens e. Scavengers
13.All of the following induce fever EXCEPT a. IL-12. b. IL-6. c. IL-1. d. TNF-alpha.
14.Which of the following is NOT associated with mobilization of neutrophils to infected tissue? a. TNF-alpha production by macrophages b. upregulation of selectins on blood vessel endothelium c. interferon response d. generation of a CXCL8 gradient e. proteolysis of basement membrane
15.Which of the following pairs is mismatched? a. primary granules: azurophilic granules b. secondary granules: unsaturated lactoferrin c. azurophilic granules: myeloperoxidase d. gelatinase: iron sequestration e. tertiary granules: natural killer cells.
16.The pH of the phagosome increases following phagocytosis because
a. the microbe delivers a significant number of hydroxyl ions in its cytosol that are released upon membrane disruption. b. hydrogen ions are consumed by the activity of NADPH oxidase and superoxide dismutase. c. azurophilic granules deliver alkaline substances. d. catalase consumes hydrogen ions once activated.
17.C-reactive protein binds to a. phosphorylcholine. b. mannose-containing carbohydrates. c. lipoteichoic acid. d. flagellin. e. MASP-1/MASP-2.
18.The C3 convertase that functions in the lectin pathway of complement activation consists of a. C3bBb. b. C3b2a. c. C4b2a. d. C4b2b. e. C3b2Bb.
19.Which of the following cleaves C2? a. Factor B b. C1r c. MASP-2 d. C4b2a e. C4b
20.With which of the following complement proteins does C-reactive protein interact? a. factor D b. C1
c. factor P d. C4 e. C2
21.All of the following are true of MyD88 EXCEPT a. it binds to the TIR domains of all Toll-like receptors except TLR3. b. it binds to IRAK4, a protein kinase, causing the kinase to phosphorylate itself. c. it is an adaptor protein with similar function to TRIF. d. a genetic deficiency of MyD88 causes the disease X-linked ectodermal dysplasia and immunodeficiency.
22.The name given to cytokines that recruit cells to move toward areas of inflammation is a. chemokines. b. caspase-recruitment domains (CARDs). c. inflammakines. d. adhesion molecules. e. pyrogens.
23.In common with Toll-like receptors, NOD-like receptors also contain __________ that is/are used for pathogen-recognition of microbial ligands. a. caspase-recruitment domains (CARD) b. Toll interleukin 1 receptor (TIR) domain c. variable extracellular domain d. leucine-rich repeat regions (LRRs) e. C-type lectin domain (CTLD)
24.Identify which of the following receptors lead to nuclear translocation of NF\kappaB through an activated IKK intermediates. a. TLR4 b. IL-1 receptor c. NOD1
d. NOD2 e. All of these receptors culminate in nuclear translocation of NF\kappaB through an activated IKK intermediate.
25.Which of the following is most similar in its activity to that of IRF3? a. IRAK4 b. NF\kappaB c. TRAF6 d. I\kappa\kappa e. GTP-binding (G) protein
26.__________ help to prevent systemic bacterial dissemination by producing chromatin structures loaded with antimicrobial substances. a. Inflammasomes b. Neutrophil extracellular traps c. RIG-1-like helicases d. Granulomas e. Plasmacytoid dendritic cells
27.__________ is/are needed to minimize the damaging effects to neighboring host cells during a respiratory burst. a. Catalase activity b. Complement control proteins c. NADPH oxidase activity d. Neutrophil mobilization e. C reactive protein
28.Measurement of which of the following is commonly used when monitoring patients for infection or inflammation? a. IL-1RA b. cryopyrin c. C-reactive protein d. proIL-1\beta
e. IL-15
29.All of the following characterize serum amyloid protein EXCEPT a. it can activate cells to produce inflammatory cytokines. b. it interacts with CD36 scavenger receptor. c. it increases in concentration by 25 percent or more in response to infection. d. it associates with high-density lipoprotein particles. e. it activates the classical pathway of complement activation.
30.__________ is not an opsonin. a. Mannose-binding lectin b. IFN-\alpha c. C-reactive protein d. Surfactant protein-A (SP-A) e. Surfactant protein-D (SP-D)
31.Toll-like receptors are located a. only on the plasma membrane. b. on the plasma membrane and the mitochondrial outer membrane. c. on the plasma membrane and endosomal membranes. d. only in the cytoplasm. e. inside inflammasomes.
32.Toll-like receptors differ from scavenger receptors in that they a. bind to common repetitive arrays on microbial surfaces. b. stimulate a pathway that causes enzymatic degradation of the microbe to which they bind. c. are soluble receptors that bind to microbes in extracellular spaces. d. mediate signal transduction pathways, causing cytokine production.
33.The Toll-like receptor that is able to signal through both the TRIF and MyD88 pathways is
a. TLR3. b. TLR4. c. TLR7. d. TLR8. e. TLR9.
34.Unlike inflammatory cytokines, Toll-like receptors a. are never secreted. b. participate only in adaptive immune responses. c. are expressed only by dendritic cells. d. stimulate the production of acute-phase proteins. e. induce fever.
35.All of the following statements regarding Toll-like receptors are true EXCEPT a. they exist as either transmembrane homodimers or heterodimers. b. the extracellular domain detects the microbial component. c. they facilitate changes in gene expression. d. they sense molecules not found in or on human cells. e. the cytoplasmic signaling domain contains a variable number of leucine-rich repeat regions (LRRs).
36.__________ binds to and retains NFκB in the cytosol. a. MyD88 b. TRAF6 c. I\kappaB d. I\kappa\kappa e. IRAK4
37.Plasmacytoid dendritic cells a. detect viral infection by using TLR4. b. produce large amounts of the type I interferons when activated. c. are found exclusively in the blood.
d. make up 10 percent of circulating leukocytes. e. have a cytoplasmic morphology resembling that of a resting B cell.
38.All of the following are correct in reference to type I interferons EXCEPT a. type I interferons inhibit the replication of viruses. b. in the presence of type I interferons, virus-infected cells undergo cellsurface changes that render them more susceptible to attack by NK cells. c. not only can most cells synthesize type I interferons, but they can also respond to them. d. the receptor for type I interferons is abundant in the cytosol and absent on the cell surface. e. type I interferons promote NK-cell proliferation and differentiation into cytotoxic cells.
39.The following cytokines activate NK cells early in the course of a viral infection with the exception of a. IFN-\alpha. b. IFN-\beta. c. IFN-\gamma. d. IL-12. e. IL-15.
40.The function of uterine NK cells (uNK) is to a. kill virus-infected cells. b. secrete growth factors that promote blood vessel growth to supply the placenta. c. activate resident macrophages by secreting inflammatory cytokines. d. secrete 1,000 times more type I interferon than other cells to protect the fetus from viral infection.
41.NK cells express each of the following proteins either on endosome membranes or on their cell surface with the exception of a. CD3.
b. type I interferon receptor. c. CD56. d. LFA-1.
42.Natural killer cells a. express either activating or inhibitory receptors on the cell surface, but not both. b. lack receptors for IL-12, thus preventing host tissue damage. c. perform the same function in the blood and in tissues such as the uterus. d. express Toll-like receptors allowing them to respond to viral RNA. e. All of these answers are correct.
43.Which of the following describes a safety mechanism to ensure that only infected cells are attacked by NK cells? a. The default state for NK cells is one of activation, which is overcome by the binding of inhibitory ligands. b. NK cells are able to secrete cytotoxic enzymes and proteins, thus killing multiple infected cells from a distance. c. No single receptor–ligand interaction induces cytotoxicity, but instead many combinations of receptor–ligand interactions influence the decision to kill or not to kill a target cell. d. NK cells express the receptor NKG2C, which limits NK cell activation.
44.Which of the following does NOT describe a feature observed when a target cell is induced to commit apoptosis by an NK cell? a. DNA fragmentation by target cell nucleases b. target cell shrinkage c. shedding of membrane-enclosed vesicles by the target cell d. chromatin extrusion in the form of decondensed DNA by the target cell e. macrophage disposal of apoptotic remains of the target cell.
45.Which of the following set of Toll-like receptors are expressed in NK cells? a. TLR3, TLR7, TLR8
b. TLR2, TLR4, TLR5, c. TLR2, TLR4, TLR9 d. TLR7 and TLR8 e. NK cells express all 10 Toll-like receptors
46.Immediately after engagement of NK-cell Toll-like receptors, the NK cell a. discharges cytotoxic granules. b. ligates IL-12R\beta1 and IL-12R\beta 2. c. synthesizes and secretes IL-15. d. synthesizes and secretes IL-12. e. synthesizes and secretes type I interferons.
47.Stimulation of NK cells by IL-12 a. is sufficient to cause the NK cell to produce large amounts of IFN-gamma. b. skews their differentiation into effector NK cells. c. induces the synthesis and secretion of IL-15 by NK cells. d. turns off type I interferon production by NK cells. e. induces the NK cell to undergo programmed cell death.
48.__________ is a cytokine produced by both macrophages and dendritic cells that promotes the proliferation, differentiation, and survival of NK cells. a. IL-15 b. IL-1\beta c. CXCL8 d. TNF-\alpha e. IL-6
49.Virally infected myeloid dendritic cells a. are not able to be detected or killed by NK cells. b. may release IL-15, activating macrophages to kill the virally infected cells. c. may outnumber NK cells and migrate to secondary lymphoid tissues. d. are unable to migrate to secondary lymphoid tissues.
e. secrete cytokines that allow the migration of NK cells to secondary lymphoid tissue.
50.After recognizing its ligand, a NOD receptor interacts with a signaling protein called __________, which is a serine–threonine kinase that phosphorylates TAKI. a. CARD b. NLRP3 c. RIPK2 d. MARCO e. SR-A
51.An adaptor protein in the inflammasome is required to link __________ to the NOD-like receptor NLRP3. a. MyD88 b. procaspase-1 c. RIPK2 d. TAKI e. IKK
52.Chemokine receptors form complexes with __________ after binding to their ligands. a. inflammasome components b. pro-IL-1\beta c. potassium channels d. GTP-binding proteins e. tertiary granules
53.All of the following acute-phase proteins increase in concentration in the plasma during inflammation with the exception of a. albumin. b. serum amyloid A protein. c. fibrinogen. d. C3.
e. mannose-binding lectin.
54.The ligands of endosomal Toll-like receptors are a. lipids of Gram-negative bacteria. b. flagellin proteins of bacteria. c. lipids of Gram-positive bacteria. d. zymosan of fungi. e. nucleic acids of viruses and bacteria.
55.Of the following Toll-like receptors, which is the most highly conserved and displays the smallest amount of allelic polymorphism? a. TLR1 b. TLR8 c. TLR10 d. TLR6 e. TLR4
56.Sensors for viral nucleic acid in the cytoplasm, called RLRs, possess domains that bind to a. GTP-binding proteins. b. type 1 interferons. c. the 5’ cap of messenger RNA (mRNA). d. oligomerized procaspase-1. e. CARD domains of MAVS.
57.What is the name given to the earliest intracellular vesicle that contains material opsonized by macrophages? a. opsonome b. membrane-attack complex c. lysosome d. phagosome e. phagolysosome
58.Which of the following activities are most closely associated with natural killer cells? a. production of TNF-α b. lysis of virus-infected cells c. phagocytosis of bacteria d. release of reactive oxygen intermediates e. formation of extracellular traps
59.The lectin pathway of complement activation is induced by a. C-reactive protein. b. antibodies bound to pathogens. c. mannose-binding lectin. d. iC3Bb. e. terminal components of the complement pathway.
60.Which of the following is NOT a characteristic of mannose-binding lectin? a. acts as an opsonin by binding to mannose-containing carbohydrates of pathogens b. synthesized by hepatocytes c. induced by elevated IL-6 levels d. triple helix of protein-forming, multiple ligand-binding sites e. triggers the alternative pathway of complement activation
61.Which of the following is NOT a characteristic of C-reactive protein? a. acts as an opsonin by binding to phosphorylcholine of pathogens b. synthesized by spleen c. induced by elevated IL-6 levels d. a member of the pentraxin family e. triggers the classical pathway of complement activation
62.Which of the following TLRs do not use a signal transduction cascade involving
MyD88? a. TLR1:TLR2 b. TLR3 c. TLR4 d. TLR2:TLR6 e. TRL7
63.Which of the following adaptor proteins participates in the activation pathway induced through either TLR3 or TLR4 that culminates in the synthesis of type I interferons? a. C-reactive protein b. MyD88 c. LPS-binding protein d. TRIF e. NF-κB
64.Which of the following properties is common to macrophages and neutrophils in an uninfected individual? a. life-span b. anatomical location c. ability to phagocytose d. morphology e. formation of pus
65.Which of the following best describes an endogenous pyrogen? a. cytokines made by pathogens that decrease body temperature b. pathogen products that decrease body temperature c. pathogen products that increase body temperature d. cytokines made by the host that decrease body temperature e. cytokines made by the host that increase body temperature
66.Which of the following is an acute-phase protein that enhances complement fixation?
a. TNF-\alpha b. mannose-binding lectin c. fibrinogen d. LFA-1 e. CXCL8
67.Inflammation a. is dependent on antibodies activating complement. b. can lead to fever and swelling. c. may result in damage to host tissue. d. may occur when a pathogen bypasses the protective epithelial surfaces and immediate immune defenses. e. includes the recruitment of white blood cells to site of infection.
68.Select the correct response using the information shown in the figure.
a. The cell labeled “A” is most likely recognizing a viral glycoprotein on the infected cell’s surface. b. The cell labeled “B” is categorized as “non-self.” c. The bacterial components labeled “C” likely resemble “self” molecules and
are thus able to be recognized by the macrophage. d. The molecules labeled “D” are categorized as “altered-self.” e. None of these answers are correct.
69.Pro-IL-1β a. is secreted by activated macrophages. b. is produced by neutrophils after TLR activation. c. is cleaved by procaspase 1. d. is cleaved and may lead to pyroptosis. e. All of these answers are correct.
70.The common lymphocyte precursor cell a. gives rise to lymphocytes involved in adaptive immunity only. b. gives rise to both the ILCs and NK cells. c. is located in the lymph nodes. d. is not needed for the development of NK cells. e. gives rise to cells that are able to fight viral infections, but not bacterial infections.
71.During an infection in the gut with large multicellular parasites a. NK cells would first respond followed by ILCs. b. ILC1 cells would respond. c. ILC2 cells would respond. d. ILC cells secreting IL-17 would respond.
72.Which of the following statements is INCORRECT concerning the process of neutrophils accessing infected tissues? a. Neutrophils respond to a chemokine gradient at the site of infection. b. Neutrophils move between blood endothelial cells via diapedesis. c. LFA-1 on neutrophils binds ICAM-1 in a process of rolling adhesion, and this interaction is followed by selectin binding to addressins. d. Neutrophils that have entered the tissues may activate NADPH oxidase.
e. In the absence of infection, neutrophils remain in the blood.
73.Match the term with its correct description. a. interferon response b. apoptosis c. extravasation d. respiratory burst e. acute-phase response 1. __________ a notable rise or reduction of plasma proteins in response to IL-6 2. __________ stimulates inhibition of viral replication 3. __________ temporary rise in oxygen consumption and toxic oxygen species production 4. __________ cellular suicide characterized by DNA fragmentation 5. __________ migration of neutrophils into inflamed tissues
74.Match the condition/disease with its correct description. a. X-linked hypohidrotic ectodermal dysplasia and immunodeficiency (NEMO deficiency) b. septic shock c. chronic granulomatous disease d. increased susceptibility to herpesvirus infections 1. __________ insufficient superoxide production in neutrophils compromises the respiratory burst 2. __________ failure to translocate NF\kappaB and activate macrophages due to deficiency in IKK/gamma subunit 3. __________ allelic polymorphism of TLR4 with glycine at position 299 causing reduced responsiveness to LPS of Gram-negative bacteria 4. __________ natural killer cell deficiency
75.Match the term with its correct description. a. oligoadenylate synthetase b. plasmacytoid dendritic cell (PDC) c. RIG-I-like helicase d. protein kinase R (PKR) e. NK-cell synapse