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T cell
depletion and no effect of 
T cell depletion
a Innere Medizin II,
Medizinische Klinik, Universitätskliniken des Saarlandes, D-66421
Homburg/Saar, Germany, b Zentrum Anatomie, Medizinische Hochschule
Hannover, D-30623 Hannover, Germany
Correspondence to: Dr J C Hoffmann, Medizinische Klinik I, Universitätsklinikun Benjamin Franklin Hindenburgdamm 30, D12200 Berlin, Germany. JC-Hoffman{at}t-online.de
Accepted for publication 14 November 2000
BACKGROUND AND
AIM
Indirect evidence suggests that
CD4+ T cells have a pathogenic while 
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, 
T cells,
or T cells.
METHODST helper
cells, T cells, or 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
T cell receptor (R73), and the T cell receptor (V65).
Depletion was verified by flow cytometry and/or immunohistology. Colitis was induced using intracolonic application of TNBS.
RESULTSSurprisingly,
depletion of T helper cells or T cells had no influence on
survival, macroscopic or microscopic scores, or myeloperoxidase
activity following colitis induction. In contrast, depletion of
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 T cell depleted group compared
with controls (p<0.05).
CONCLUSIONST helper
cells or T cells did not influence the initiation or
perpetuation of rat TNBS colitis. In contrast, T cells had a
protective role in rat TNBS colitis as depletion caused increased mortality.
T cells;
T cells;
experimental
colitis;
inflammatory bowel disease;
rat
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