Chapter Category: Autoimmunity

From the book Immune Mechanisms in Inflammatory Bowel Disease

Alterations of T Lymphocytes in Inflammatory Bowel Diseases

Charles O. Elson, Yingzi Cong and Casey T. Weaver

The intestine contains an abundance of cells of the innate and acquired immune system, and among these T cells represent a major component. Intestinal T cells are distributed among the various compartments in the mucosal immune system, including GALT, the epithelial layer, and the lamina propria. Intestinal T cells are quite distinct from peripheral T cells in phenotype and function, however there have been remarkably few differences between T cells isolated from normal vs inflamed mucosa, perhaps because the ‘normal’ gut is in a state of low grade inflammation.1,2 Most studies on intestinal T cells focus on human or mouse isolates and there can be some significant species differences between these two. Secondly, one should keep in mind that human “lamina propria” isolates are actually mixtures of true lamina propria lymphocytes plus cells from the abundant microscopic lymphoid follicles that are present throughout the human intestine. Lamina propria (LP) T cells have been most studied in humans with or without IBD (Table 1).3 The ratio of CD4+ to CD8+ T cells is 2:1, similar to peripheral blood. Most lamina propria T cells bear ab T cell receptors, express activation markers, and are CD45RO+ memory cells. Despite these features, LP T cells proliferate poorly to stimulation via the T cell receptor/CD3 complex. Rather, they respond preferentially to stimulation via TCR ligation plus costimulation via CD2 and CD28.4 The reason for this shift in TCR-mediated pathways is unclear but may be due to the presence of a soluble factor in the LP microenvironment. LP T cells can produce cytokines when stimulated in vitro, but do not produce detectable cytokines in situ. Even in progressive, fatal experimental colitis mediated by CD4+ T cells, only a few CD4+ T cells per thousand are actively producing cytokines in situ at any one time.5,6

Taken from the book

Immune Mechanisms in Inflammatory Bowel Disease

Edited by: Richard S. Blumberg and Markus F. Neurath

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