Role of T lymphocytes in rat 2,4,6-trinitrobenzene sulphonic acid (TNBS) induced colitis: increased mortality after gammadelta T cell depletion and no effect of alphabeta T cell depletion

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Abstract
BACKGROUND AND AIM Indirect evidence suggests that CD4+ T cells have a pathogenic while γδ T cells have a protective role in the initiation and perpetuation of inflammatory bowel disease. To define the role of T cell subsets in a rat colitis model (2,4,6-trinitrobenzene sulphonic acid (TNBS)) we analysed colitis severity after effective depletion of T helper cells, αβ Τ cells, or γδ T cells. METHODS T helper cells, αβ T cells, or γδ T cells were depleted using previously described monoclonal antibodies directed at the CD4 molecule (OX38), the CD2 molecule (OX34, both depleting CD4+ T cells), the αβ T cell receptor (R73), and the γδ T cell receptor (V65). Depletion was verified by flow cytometry and/or immunohistology. Colitis was induced using intracolonic application of TNBS. RESULTS Surprisingly, depletion of T helper cells or αβ T cells had no influence on survival, macroscopic or microscopic scores, or myeloperoxidase activity following colitis induction. In contrast, depletion of γδ T cells resulted in significantly increased mortality (V65: 73%, n=15) compared with controls (30%, n=13; pCONCLUSIONS T helper cells or αβ T cells did not influence the initiation or perpetuation of rat TNBS colitis. In contrast, γδ T cells had a protective role in rat TNBS colitis as depletion caused increased mortality.

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