Open AccessT cell receptor repertoire and mitotic responses of lamina propria T lymphocytes in inflammatory bowel disease
Author(s) -
QIAO L.,
GOLLING M.,
AUTSCHBACH F.,
SCHURMANN G.,
MEUER S. C.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06085.x
Subject(s) - lamina propria , immunology , inflammatory bowel disease , biology , mitosis , receptor , repertoire , disease , medicine , pathology , microbiology and biotechnology , genetics , epithelium , physics , acoustics
SUMMARY Human intestinal lamina propria T lymphocytes (LPL‐T) physiologically exhibit minimal proliferation in response to antigen receptor stimulation in vitro . This is thought to occur as a consequence of regulatory influences which are exerted by the mucosal microenvironment. The present study is aimed at investigating whether proliferative responses of intestinal LPL‐T to antigen receptor stimulation are altered in patients with inflammatory bowel disease. Accordingly, proliferative responses of LPL‐T in patients with Crohn's disease and ulcerative colitis to stimulation with CD3 MoAb plus IL‐2 were examined and compared with controls. In addition, T cell receptor (TCR) repertoires of LPL‐T and peripheral blood T lymphocytes were determined by indirect immunofluorescenee using a panel of 11 TCR Vβ specific antibodies. In most patients with inflammatory bowel disease, LPL‐T showed enhanced proliferation to antigen receptor stimulation compared with controls. Moreover, perhaps as a consequence, an enhanced frequency of in vivo preactivated T cells was seen as judged from an increased spontaneous proliferative response to low concentrations of exogenous IL‐2. LPL‐T and peripheral blood T lymphocytes exhibited similar percentages of TCR Vβ gene usage both in controls and in patients. In summary, polyclonal activation of LPL‐T due to impairment of local adjustment, i.e. insufficient down‐regulation of TCR/CD3‐dependent signalling processes, may contribute to the pathogenesis of inflammatory bowel disease.