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The interactive role of mucosal T lymphocytes in intestinal growth, development and enteropathy

1993; Wiley; Volume: 8; Issue: 3 Linguagem: Inglês

10.1111/j.1440-1746.1993.tb01199.x

1440-1746

Michael N. Marsh, Adrian G. Cummins,

Eosinophilic Esophagitis

Abstract Over the past 15–20 years, research has progressively focused on the mucosal T cell as the central factor in the initiation of physiological or pathological changes, first in the growth and maturation of the early (postnatal) intestine, and second in adult‐type enteropathies resulting from sensitivity to either food or pathogen‐derived antigens. T cell‐mediated events may be measured, for example, in terms of specific immunopathologic patterns of change and injury, such as type 1 (lymphocyte infiltration), type 2 (crypt hyperplasia) and type 3 (flat‐destructive), which can be recognized and quantitated microscopically; by determination of lymphocyte reactivity through secretion of interleukin‐2 receptors (IL‐2R) into plasma or expression by mucosal lymphocytes; by quantitation of lymphocyte subsets emigrating into inflamed tissues by immunoperoxidase‐labelled monoclonal antibodies; or by the determination of T cell receptor polymorphisms. Alterations in intestinal growth, structure and function at weaning are likely to be T cell‐mediated as they are analogous to the same type 1/2 lesions that reflect modulation of adult mucosal architecture in food and parasite‐induced hypersensitivity reactions. Enteropathies associated with HIV infection and T cell deficiency display a milder degree of villous flattening and impaired crypt hyperplasia than that typical of gluten‐sensitivity, suggesting a reversion to lesser degrees of mucosal pathology (type 1/2). Clearly more information will accrue; meanwhile the remarks in this brief survey should provide a firm basis whereby clinician and scientist can meet, and together recognize and further dissect the modulatory effect of T lymphocytes on mucosal structure and function.