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

Authors
  • J Hoffmann
  • K Peters
  • S Henschke
  • B Herrmann
  • K Pfister
  • J Westermann
  • M Zeitz
Publication Date
Apr 01, 2001
Source
PMC
Keywords
Disciplines
  • Biology
  • Medicine
License
Unknown

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 T 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; p<0.03). In addition, colitis was histologically more severe in the γδ T cell depleted group compared with controls (p<0.05).
CONCLUSIONS—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.


Keywords: αβ T cells; γδ T cells; experimental colitis; inflammatory bowel disease; rat

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