Chapter 3 : Intestinal Immunity

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Intestinal immunity is a relatively new term in relation to events and processes that precede human biology. Antigens need to be sampled, processed, and presented in such a way that enables the destruction of pathogens and tolerance of nonpathogens. Therefore, the rules governing intestinal immunity differ from those observed in systemic immunity. Cells of the gut-associated lymphoid tissue (GALT) include conventional cells of the innate and adaptive immune system such as B and T lymphocytes, macrophages, and dendritic cells (DC), as well as more unusual antigen-presenting cells (APC) and lymphocytes unique to the GALT, such as intestinal epithelial cells (IEC), lamina propria lymphocytes (LPL), and intraepithelial lymphocytes (IEL). These cells have unique activation requirements, and they secrete, and are influenced by, a special array of cytokines and mediators. These unique cells and phenomena are discussed in this chapter. Tight junctions between epithelial cells function as potent exclusion barriers for large macromolecules or pathogens. Increasing evidence suggests that CD8 regulatory T cells are stimulated in the GALT after interaction with IEC or DC. In certain inflammatory states, however, the function of tight junctions is disturbed, thus enabling the transit of charged molecules, bacteria, and nutrients across the epithelium. LPL are a very heterogeneous group composed of T and B cells, as well as plasma and mast cells and macrophages.

Citation: Dotan I, Mayer L. 2003. Intestinal Immunity, p 43-59. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch3
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The interaction of IEC with T cells—a suggested model. IEC express a variety of surface molecules relevant for antigen presentation and stimulation of T cells (see Table 2). Luminal antigens derived from food or bacteria may be internalized via the apical surface. In the presence of inflammation, paracellular transport of antigens and presentation by basolateral surface molecules may occur. The amount and type of antigen, as well as the combination of antigen-presenting molecules with costimulatory molecules, determine the population of T cells that will expand. CD8 IEL and LPL may be stimulated by classical MHC class I molecules. Stimulation by class I-like molecules, such as the complex gp180:CD1d and MICA/MICB, may also occur. The antigen presented in the IEC:CD8 T-cell interaction is of nonpeptide origin. When presented by CD1d, data suggest it is a bacterial-derived phospholipid. The nature of antigen presented to CD8 T cells by MICA/MICB expressing IEC remains hypothetical at this point. CD8 T cells activated by IEC have a suppressor activity and may function in regulating mucosal homeostasis. Peptide antigens can be presented to CD4 T cells by MHC class II molecules, which are constitutively expressed on IEC. Different CD4 T-cell populations may expand when the antigen is taken up via the apical or the basolateral surface. In normal mucosal homeostasis, regulatory CD4 T cells, activated via MHC class II without costimulation, may contribute to controlled inflammation. In inflammatory states, upregulation of MHC class II as well as costimulatory molecules such as CD86 may promote the expansion of TH1/TH2 cells and contribute to uncontrolled inflammation.

Citation: Dotan I, Mayer L. 2003. Intestinal Immunity, p 43-59. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch3
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Generic image for table

Innate and adaptive immunity in the gut

Citation: Dotan I, Mayer L. 2003. Intestinal Immunity, p 43-59. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch3
Generic image for table

IEC express surface molecules that are relevant to antigen processing and presentation to T cells

Citation: Dotan I, Mayer L. 2003. Intestinal Immunity, p 43-59. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch3

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