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Mucosal Immunity

Local immunity refers to immunologic reactivity confined principally to a particular anatomic site such as the respiratory or gastrointestinal tract. Local antibodies as well as lymphoid cells present in the area may mediate a specific immunologic effect. For example, secretory IgA produced in the gut may react to food or other ingested antigens. The mucosal immune system describes aggregates of lymphoid tissues or lymphocytes near mucosal surfaces of the respiratory, gastrointestinal, and urogenital tracts (Figure 15.1 to Figure 15.4). There is local synthesis of secretory IgA and T cell immunity at these sites. The mucosal epithelial layer serves as a mechanical barrier against foreign antigens and invading microorganisms. A specialized immune system, sometimes referred to as the common mucosal immune system (CMIS), located at epithelial surfaces, represents a critical defense mechanism. The mucosal immune system consists of secretory IgA molecules produced by plasma cells in the lamina propria and subsequently transported across epithelial cells with the aid of the polyimmunoglobulin receptor. Both αβ and γδ T lymphocytes are present in the mucosal epithelial layer as intraepithelial lymphocytes. They are also found in the lamina propria of the mucosa, where they serve as an integral component of the cellular immune system. These T lymphocytes function in the induction and regulation of responses by antigen-specific IgA B cells as well as effector T cells. The epithelial cells lining mucosal surfaces furnish signals that are significant for the initiation of the mucosal inflammatory response and critical communications between epithelial cells and mucosal lymphoid cells. The immune response to oral antigens differs from the response to parenterally administered immunogens. Oral tolerance may follow the ingestion of some protein antigens, but a vigorous local mucosal immune response with the production of high concentrations of IgA may follow oral immunization with selected vaccines such as the Sabin oral polio vaccine. Mucosa-associated lymphoid tissue (MALT) includes extranodal lymphoid tissue associated with the mucosa at various anatomical sites, including the skin (SALT), bronchus (BALT), gut (GALT), nasal associated lymphoid tissue (NALT), breast, and uterine cervix. The mucosa-associated lymphoid tissues provide localized or regional immune defense since they are in immediate contact with foreign antigenic substances, thereby differing from the

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lymphoid tissues associated with lymph nodes, spleen, and thymus. Secretory or exocrine IgA is associated with the MALT system of immunity. The lymphoid tissues comprising MALT include intraepithelial lymphocytes, principally T lymphocytes, together with B cells beneath the mucosal epithelia and in the lamina propria. Gut-associated lymphoid tissue (GALT) describes lymphoid tissue in the gastrointestinal mucosa and submucosa. It constitutes the gastrointestinal immune system (Figure 15.5). GALT is present in the appendix, in the tonsils, and in the Peyer’s patches subjacent to the mucosa. GALT represents the counterpart of BALT and consists of radially arranged and closely packed lymphoid follicles which impinge upon the intestinal epithelium, forming dome-like structures. In GALT, specialized epithelial cells overlie the lymphoid follicles, forming a membrane between the lymphoid cells and the lumen. These cells are called M cells. They are believed to be “gatekeepers” for molecules passing across. Other GALT components include IgA-synthesizing B cells and intraepithelial lymphocytes such as CD8+ T cells, as well as the lymphocytes in the lamina propria that include CD4+ T lymphocytes, B lymphocytes which synthesize IgA, and null cells. The lamina propria is the thin connective tissue layer that supports the epithelium of the gastrointestinal, respiratory, and genitourinary tracts (Figure 15.6). The epithelium and lamina propria form the mucous membrane. The lamina propria may be the site of immunologic reactivity in the gastrointestinal tract, representing an area where lymphocytes, plasma cells, and mast cells congregate. A polyimmuoglobulin receptor is an attachment site for polymeric immunoglobulins located on epithelial cell and hepatocyte surfaces that facilitate polymeric IgA and IgM transcytosis to the secretions. After binding, the receptor immunoglobulin complex is endocytosed and enclosed within vesicles for transport. Exocytosis takes place at the cell surface where the immunoglobulin is discharged into the intestinal lumen. A similar mechanism in the liver facilitates IgA transport into the bile. The receptor–polymeric immunoglobulin complex is released from the cell following cleavage near the cell membrane. The receptor segment that is bound to the polymeric immunoglobulin is known as the secretory component, which can only be used once in the transport process.

Lymphocytes in the gastrointestinal mucosa may be present in the lamina propria, Peyer’s patches, and the epithelial layer. In humans, the intraepithelial lymphocytes are mostly CD8+ T cells. γδ T cells make up these intraepithelial lymphocytes to varying degrees according to the species but constitute approximately 10% in humans. The γδ as well as the αβ intraepithelial T cells have restricted specificities probably corresponding to Ag 1. Digestive tract



Lactating breast


Intestine 3. Peyer’s patch

Respiratory tract


9. Genitourinary tract 8.

Lacrimal glands


7. Salivary glands

Mesenteric lymph node via lymphatic drainage

Plasma cells

6. Blood stream

antigens frequently found in the gut. Numerous activated B cells, plasma cells, activated CD4+ T cells, eosinophils, macrophages, and mast cells are present in the lamina propria of the intestine. T cells are believed to interact with antigen in regional mesenteric lymph nodes and then return to the intestinal lamina propria. Mucosa homing is a selective return of immunologically reactive lymphoid cells that originated in mucosal follicles, migrated to other anatomical locations, and then returned to their site of origin in mucosal areas. Receptors on lymphoid cells and ligands on endothelial cells are responsible for the cellular migration involving the mucosal immune system (Figure 15.7). MadCAM-1 is a mucosal addressin cell adhesion molecule-1 which is an addressin in Peyer’s patches of mice (Figure 15.8). This three-Ig domain structure with a polypeptide backbone binds the α4β7 integrin. MadCAM1 facilitates access of lymphocytes to the mucosal lymphoid tissues, as in the gastrointestinal tract. Addressin is a molecule such as a peptide or protein that serves as a homing device to direct a molecule to a specific location. Lymphocytes from Peyer’s patches home to mucosal endothelial cells bearing ligands for the lymphocyte homing receptor.

FIGURE 15.1 Secretory immune system. Antigen application

Inductive sites

Local draining lymph nodes

Thoracic duct

Blood stream

Effector sites

Immune memory cells home to inductive sites?







? i.r.

Lymphoid follicules in rectum


Inductive site?

Central CLN

Nasal mucosae Salivary glands

Hilar lymph nodes

Trachea and bronchi

Mesenteric lymph nodes


Rectal lymph nodes

Does not favor inducing mucosal responses

FIGURE 15.2 Compartmentalized common mucosal immune system.

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Genital tract or Rectal mucosae

FIGURE 15.3 The mucosal system and its cellular components.

FIGURE 15.4 Common mucosal inflammatory pathway.

FIGURE 15.5 GALT (gut-associated lymphoid tissue). L-Selectin is a molecule found on lymphocytes that is responsible for the homing of lymphocytes to lymph node high endothelial venules. L-Selectin is also found on neutrophils where it acts to bind the cells to activated endothelium early in the inflammatory process. L-Selectin is also called CD62L.

Mucosal lymphoid follicles include such structures as Peyer’s patches in the small intestine and pharyngeal tonsils. The appendix and other areas of the gastrointestinal tract and respiratory tract contain similar aggregrates of lymphoid cells. Germinal centers at the center of lymphoid follicles have an abundance of B cells. CD4+ T cells are

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present in interfollicular regions of Peyer’s patches. Onehalf to three quarters of the lymphocytes in murine Peyer’s patches are B cells, whereas 10 to 30% are T lymphocytes. M cells overlying Peyer’s patches are membranous (M) cells devoid of microvilli, are pinocytic, and convey macromolecules to subepithelial tissues from the lumen of the intestine. Although M cells are believed to transport antigens to Peyer’s patches, they do not act as antigen-presenting cells. Lymphoid cells in the blood migrate to the gut mucosa. The integrin α4 associated β7 is critical for endothelial binding of lymphocytes in the intestine and migration of cell into the mucosa. The M cell is a gastrointestinal tract epithelial cell that conveys microorganisms and macromolecular substances from the gut lumen to Peyer’s patches. M cells are nonantigen-presenting cells found in the epithelial layer of the Peyer’s patches that, nevertheless, may have an important role in antigen delivery. They have relatively large surfaces with microfolds that attach to microorganisms and macromolecular surfaces. The M cell cytoplasmic processes extend to CD4+ T cells underneath them. Materials attached to microvilli are conveyed to coated pits and moved to the basolateral surface, which has pronounced invaginations rich in leukocytes and mononuclear phagocytes. Thus, materials gaining access by way of M cells come into contact with lymphoid cells as they reach the basolateral surface. This is believed to facilitate induction of immune responsiveness. The term “microfold cells” refers to M cells. Lymphocytes present in the intestinal epithelium or other specialized epithelial layers are termed intraepithelial lymphocytes.

FIGURE 15.6 Lamina propria.

FIGURE 15.7 Cell traffic.

Inductive sites are small patches of mucous membrane that overlie organized lymphoid follicles and contain M cells. MIC molecules are MHC class I-like molecules expressed in the gastrointestinal tract during stress. Genes within the class I region of the human MHC encode these molecules. The secretory immune system is a major component of the immune system that provides protection from invading microorganisms at local sites. Much of the effect is mediated by secretory IgA molecules in the secretions at the mucosal surface. Immunoglobulins may also be in clotted fluids where they protect against microorganisms.

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FIGURE 15.8 MadCAM-1.

Immune exclusion describes prevention of antigen entry into the body by the products of a specific immune response, such as the blocking of an antigen’s access to the body by mucosal surfaces when secretory IgA specific for the antigen is present. Secretory IgA (Figure 15.9) is a dimeric molecule comprised of two IgA monomers joined by a J polypeptide chain

formed on the basolateral surface and fuse with the apical surface in contact with the intestinal lumen. Antiseptic paint is a colloquial designation for the coating effect of secretory IgA, such as that produced locally in the gut, on mucosal surfaces, thereby barring antigen access.

FIGURE 15.9 Secretory IgA.

FIGURE 15.10 Secretory component.

and a glycopeptide secretory component (Figure 15.10). This is the principal molecule of mucosal immunity. IgA is the only immunoglobulin isotype that can be selectively passed across mucosal walls to reach the lumens of organs lined with mucosal cells. Specific FcαR that bind IgA molecular dimers are found on intestinal epithelial cells. Specific FαR that bind IfA molecular dimers are found on intestinal epithelial cells. The FcαR, also known as secretory (S protein), joins the antibody molecule to the epithelial cell’s basal surface that is exposed to the blood. It is bound to the polyimmunoglobulin receptor on the epithelial cell’s basolateral surface and facilitates vesicular transport of the anchored IgA across the cell to the surface of the mucosa. Once this complex reaches its destination, FcαR (S protein) is split in a manner that permits the dimeric IgA molecule to retain an attached secretory piece which has a strong affinity for mucous, thereby facilitating the maintenance of IgA molecules on mucosal surfaces. The secretory piece also has the important function of protecting the secreted IgA molecules from proteolytic digestion by enzymes of the gut. These latter two functions are in addition to its active role in transporting the IgA molecule through the epithelial cell. Secretory or exocrine IgA appears in the colostrum, intestinal and respiratory secretions, saliva, tears, and other secretions. Transcytosis is the active transport of molecules across epithelial cells. IgA molecules are transported by transcytosis across intestinal epithelial cells in vesicles that are

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Secretory component (T piece) or secretory piece is a 75-kDa molecule synthesized by epithelial cells in the lamina propria of the gut that becomes associated with IgA molecules produced by plasma cells in the lamina propria of the gut (Figure 15.10) as they move across the epithelial cell layer to reach the mucosal surface of intestine to provide local immunity. It can be found in three molecular forms: as an SIgM and SIgA stabilizing chain, as a transmembrane receptor protein, and as free secretory component in fluids. Secretory piece also has the important function of protecting the secreted IgA molecules from proteolytic digestion by enzymes of the gut. These latter two functions are in addition to its active role in transporting the IgA molecule through the epithelial cell. It is also called secretory component and is a fragment of the poly-Ig receptor that remains bound to Ig following transcytosis across the epithelium and cleavage. It is not formed by plasma cells in the lamina propria of the gut that synthesize the IgA molecules with which it combines. Secretory component has a special affinity for mucous, thereby facilitating IgA’s attachment to the mucous membranes. The sacculus rotundus describes the lymphoid tissue-rich terminal segments of the ileum in the rabbit. It is a part of the gut-associated lymphoid tissue (GALT). Secretory component deficiency is a lack of IgA in secretions as a consequence of gastrointestinal tract epithelial cells’ inability to produce secretory component to be linked to the IgA molecules synthesized in the lamina propria of the gut to prevent their destruction by the proteolytic enzymes in the gut lumen. The disorder is very infrequent but is characterized by the protracted diarrhea associated with gut infection. Helicobacter pylori immunity: Both circulating and local humoral antibody responses follow H. pylori colonization of the gastric mucosa. During a prolonged mucosal infection, IgG1 and IgG4, and often, IgG2 antibodies are detectable but IgG3 and IgM antibodies only rarely. IgA antibodies are usually also present. The initial IgM response is followed later by IgA with conversion to IgG 22 to 33 days after infection. IgA antibodies are found at the local mucosal level. They are secreted into the gastric juice. IgG produced locally is rapidly inactivated when it reaches the gastric juice. A systemic IgG response is present throughout the infection and diminishes, only prolonging successful therapy. If the infection reappears, the IgG antibody titer

rises. There is great variability in the specificity of circulating host antibody against H. pylori . This is attributable in part to variations in host response and to a lesser degree to antigenic diversity of the microorganisms, such as variation in the Vac A and Cag A proteins. Most infected subjects synthesize antibodies against numerous antigens, including the urease subunits, the flagellins, and the 54-kDa hsp60 homolog. Antibodies usually develop to Vac A and Cag A polypeptides if they are present in the infecting strain. Although of variable complexity, the antigens all include urease. Plasma cells, lymphocytes, and monocytes infiltrate the superficial layers of the lamina propria in H. pylori associated gastritis. Half of the mature B cells and infiltrate are B cells that are producing mostly IgA but also IgG and IgM. These cells produce antibodies specific for H. pylori and are mostly of the CD8+ subset, although CD4+ T cells are also increased as well as γδ T cells. Gastric epithelial cells aberrantly express HLA-DR during H. pylori infection, w hich is also associated with elevated synthesis of IL-1, IL-6, and TNFα in the gastric mucosa. H. pylori induces Il-1, IL-6, and TNF-α in the gastric mucosa. It induces IL-8 expression in gastric epithelium, which induces neutrophil chemotaxis. Of the non-Hodgkins lymphoma cases affecting the stomach, 92% are associated with H. pylori infection. The bacteria may engage an immune avoidance by continually losing highly antigenic material such as urease and flagella sheath from the bacterial surface thereby diminishing the effectiveness of bound antibodies. The immune response may also be downregulated during infection as antigen-specific responsiveness of local and circulating T cells is diminished. The complexity of the disease makes development of effective vaccines difficult. An oral subunit vaccine used with a mucosal adjuvant has protected animal models. Thus immunotherapy might be a future option in prevention. Bronchial-associated lymphoid tissue (BALT) is present in both mammals, including humans, and birds (Figure 15.11).

In many areas it appears as a collar containing nodules located deep around the bronchus and connected with the epithelium by patches of loosely arranged lymphoid cells. Germinal centers are absent (except in the chicken), although cells in the center of nodules stain lighter than do those at the periphery. Plasma cells are present occasionally beneath the epithelium. The cells in BALT have a high turnover rate and apparently do not produce IgG. BALT development is independent of that of the peripheral lymphoid tissues or antigen exposure. The cells of BALT apparently migrate there from other lymphoid areas. This tissue plays an important role in mounting an immune response to inhaled antigens in respiratory infectious agents. Oral immunology: Saliva not only rinses the oral cavity but contains numerous molecules such as lysozyme and secretory immunoglobulin A which as part of the mucosal immune system help to protect the oral cavity. Polymorphonuclear leukocytes are important in protection of gingival tissues and ultimately the periodontium. In addition to secretory IgA, the systemic vascular humoral immune response is significant in oral immunity. The relative contribution of TH1 cells and TH2 cells in an immune response to plaque bacterial pathogens is significant in periodontal disease. Individuals with immunodeficiencies often have increased mucosal infections by opportunistic microorganisms, such as by Canda albicans. Immunopathologic mechanism that involve types II, III, and IV hypersensitivity may be involved in the development and progression of chronic periodontitis. Vaccines may be used in the future to prevent or control dental caries and periodontal diseases. Oral or intranasal bouts of vaccine administration may prove useful to protect against oral infections. Oral unresponsiveness is the mucosal immune system’s selective ability to not react immunologically against antigens of food and intestinal microorganisms even though it responds vigorously to pathogenic microorganisms. Oral feeding of a protein antigen may lead to profound systemic immunosuppression involving both the B cell (antibody-mediated) and T cell (cell-mediated) limbs of the immune response to that specific antigen (Figure 15.12). T cell clonal anergy is induced to some protein antigens administered by this route. Antigen presented by antigenpresenting cells deficient in costimulatory molecules may induce tolerance. Yet, possible nonprofessional antigen-presenting cells involved in the induction of oral tolerance have not been identified.

FIGURE 15.11 BALT (bronchial-associated lymphoid tissue).

Copyright © 2004 by Taylor & Francis

It has also been postulated that the immunosuppressive cytokine TGF-b may be released during the induction of oral tolerance through its ability to block lymphocyte proliferation and to induce B lymphocyte switching to IgA production. Paradoxically, it remains a mystery why large doses of soluble proteins induce systemic T lymphocyte tolerance,

FIGURE 15.12 Antigen feeding.

whereas the components of vaccines such as the Sabin polio vaccine induce an effective local immune response. Specific local immunity may be attributable to activation or infection of antigen-presenting cells in the intestinal epithelium. Nevertheless, oral tolerance is beneficial through its prevention of the body’s reaction to oral antigens or food or gastrointestinal bacteria. Feeding of autoantigen to induce oral tolerance has potential therapeutic value for the treatment of autoimmune disease. Antigen fed orally soon reaches the lymphatics of the intestine and is transported to the mesenteric lymph nodes, where it stimulates an immune response. Antigen may also reach Peyer’s patches through M cells and led to a T and B cell response. Activated lymphocytes in mesenteric lymph nodes may migrate to the lamina propria, whereas those in the Peyer’s patches may reach either the lamina propria or mesenteric lymph nodes. The epithelial layer is not only a mechanical barrier against pathogenic microorganisms but is the site in the gastrointestinal and respiratory tracts of secretory IgA antibodies. This class of immunoglobulin is also responsible for the passive transfer of immunity from mother to young through the milk and colostrum. Most of the antibodies produced in the normal adult are of the secretory IgA class. Antigens conveyed to Peyer’s patches of the intestine activate T lymphocytes and follicular B cells. IgA-synthesizing lymphocytes enter the lamina propria. IL-5 and TGF-β facilitate IgA isotype switching. Antibody affinity maturation occurs in germinal centers of Peyer’s patches where stimulated B lymphocytes have seeded and proliferated. IgA-synthesizing B lymphocytes populate the lamina propria or other mucosal tissues. The relatively large quantity of secretory IgA synthesized in tissues of the mucosal immune system is attributable to the tendency of B cells that form IgA to populate the lamina propria and Peyer’s patches. IgA-producing B lymphocytes in other parts of the body are responsible for serum IgA.

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Oral tolerance is antigen-induced specific suppression of humoral and cell-mediated immunity to an antigen following oral administration of that antigen as a consequence of anergy of antigen-specific T lymphocytes for the formation of immunosuppressive cytokines such as transforming growth factor-β. Oral tolerance may inhibit immune responses against food antigens and bacteria in the intestine. Proteins passing through the gastrointestinal tract induce antigen-specific hyporesponsiveness. Oral tolerance is believed to have evolved to permit the gut-associated immune system to be exposed to external proteins without becoming sensitized. If proteins such as ovalbumin or myelin basic protein (MBP) are fed to animals which are then immunized, the immune response against the fed antigen, but not against the control antigen, is subsequently diminished. Based on the quantity of antigen fed, orally administered antigen may induce regulatory cells that suppress the antigen-specific response (low doses) or inhibit antigen-specific T cells by induction of clonal anergy (high doses). Antigens passing through the gastrointestinal tract preferentially induce T helper (Th2)type T cells that secrete interleukin-4, IL-10, and transforming growth factor β (TGFβ). These cells migrate from the gut to organs that contain the fed antigen, where the Th2 cells are stimulated locally to release antiinflammatory cytokines. Mucosal tolerance is synonymous with oral tolerance. Maternal immunity describes passive immunity conferred on the neonate by its mother. This is accomplished prepartum by active immunoglobulin transport across the placenta from the maternal to the fetal circulation in primate animals including humans. Other species such as ungulates transfer immunity from mother to young by antibodies in the colostrum since the intestine can pass immunoglobulin molecules across its surface in the early neonatal period. The egg yolk of avian species is the mechanism through which immunity is passed from mother to young in birds.

Colostrum is immunoglobulin-rich first breast milk formed in mammals after parturition. The principal immunoglobulin is IgA with lesser amounts of IgG. It provides passive immune protection of the newborn prior to maturation of its own immune competence. Coproantibody is a gastrointestinal tract antibody, commonly of the IgA class, which is present in the intestinal lumen or feces. The Sulzberger-Chase phenomenon is the induction of immunological unresponsiveness to skin-sensitizing chemicals such as picryl chloride by feeding an animal (e.g., guinea pig) the chemical in question prior to application to the skin. Intravenous administration of the chemical may also block the development of delayed-type hypersensitivity when the same chemical is later applied to the skin. Simple chemicals such as picryl chloride may induce contact hypersensitivity when applied to the skin of guinea pigs. The unresponsiveness may be abrogated by adoptive immunization of a tolerant guinea pig with lymphocytes from one that has been sensitized by application of the chemical to the skin without prior oral feeding. Chase-Sulzberger phenomenon: See Sulzberger-Chase phenomenon. Skin immunity: The skin, the largest organ in the body, shields the body’s interior environment from a hostile exterior (Figure 15.13). The skin defends the host through stimulation of inflammatory and local immune responses. Antigen applied to or injected into the skin drains to the regional lymph nodes through the skin’s extensive lymphatic network. Cells of both the epidermis, papillary, and reticular dermis have critical roles in the skin’s immune function. Keratinocytes, which are epidermal epithelial cells, secrete various cytokines such as granulocyte–macrophage colony-stimulating factor, interleukin-1, interleukin-3, interleukin-6, and tumor necrosis factor. T lymphocytes in the skin may secrete IFN-γ or other cytokines that cause these epithelial cells to synthesize

chemokines that lead to leukocyte chemotaxis and activation. Stimulation by IFN-γ may also lead to their expression of class II MHC molecules. Other epidermal cells include Langherans cells, which form an extensive network in the epidermis that permits their interaction with any antigen entering the skin. The few lymphocytes in the epidermis are principally CD8+ T cells often with restricted antigen receptors. In the mouse, these are mostly γδ T cells. Skin lymphocytes and macrophages are mostly in the dermis. The T cells are of CD4+ and CD8+ phenotypes and often perivascular. The cutaneous immune system is comprised of adaptive and innate immune system constituents present in the skin that function in concert to detect and respond to environmental antigens. Among the cutaneous immune system constituents are keratinocytes, Langerhans cells, intraepithelial lymphocytes, and dermal lymphocytes. Intraepidermal lymphocytes are primarily CD8+ T cells within the dermis. Murine intraepidermal lymphocytes express mainly the γδ receptor. It is believed that these cells have a more restricted repertoire of antigen receptors than those homing to extracutaneous sites. Most skinassociated lymphocytes are found in the dermis with only about 2% in the epidermis. Intraepidermal lymphocytes express CLA-1, which may play a role in homing. Langerhans cells are the principal antigen-presenting cells in the skin. They encounter antigen entering through the skin and process it. Langerhans cells may reach the parafollicular cortical areas of the regional lymph nodes via lymphatic vessels of the skin. These Langerhans cells develop into effective antigen-presenting cells as a result of upregulation of class II MHC molecules and of costimulatory molecules. In the lymph nodes they present antigen to CD4+ T lymphocytes after becoming interdigitating dendritic cells. Dermal macrophages may present protein antigens to previously activated T cells. Delayed type hypersensitivity reactions are mediated by T cells in the skin reacting to soluble protein antigens or to chemicals acting as haptens that combine with self proteins producing new epitopes. This cell-mediated immune reaction is accompanied by the release of cytokines from the activated T cells. With respect to the antibody response of the skin, secretory IgA is found in sweat, which aids in defense against infection. IgE on the surface of mast cells in the dermis participates in the generation of immediate type I hypersensitivity reactions in the skin. Thy-1+ dendritic cells are found within the epithelium of the mouse epidermis.

FIGURE 15.13 The cutaneous immune system and its cellular components.

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The cutaneous lymphocyte antigen HECA-452 epitope is expressed on a skin-associated subset of memory T cells that are active in recirculation and homing to skin sites.

Cutaneous sensitization may be induced by application of antigen to the skin to induce hypersensitivity. Cutaneous T-cell lymphoma describes a malignant growth of T lymphocytes that home to the skin, such as mycosis fungoides.

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Photoimmunology is the investigation of the effects of photons on the immune system. The effects of photons on the immune system are initiated in the skin from interaction of ultraviolet radiation with immune cells. Ultraviolet-induced immune suppression may play a role in human skin cancer induction.

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