Article Text
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; 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.
- αβ T cells
- γδ T cells
- experimental colitis
- inflammatory bowel disease
- rat
Abbreviations used in this paper
- IBD
- inflammatory bowel disease
- ko
- knock out
- PALS
- periarteriolar lymphocyte sheath
- TCR
- T cell receptor
- TNBS
- 2,4,6-trinitrobenzene sulphonic acid
- Th1
- T helper 1
- mAb
- monoclonal antibody
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Abbreviations used in this paper
- IBD
- inflammatory bowel disease
- ko
- knock out
- PALS
- periarteriolar lymphocyte sheath
- TCR
- T cell receptor
- TNBS
- 2,4,6-trinitrobenzene sulphonic acid
- Th1
- T helper 1
- mAb
- monoclonal antibody