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Experimental Studies of Immunologically Mediated Enteropathy
Author(s) -
FELSTEIN M. V.,
MOWAT A. MCI.
Publication year - 1990
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1990.tb03186.x
Subject(s) - ctl* , enteropathy , cytotoxic t cell , immunology , atrophy , deoxyguanosine , hyperplasia , biology , medicine , chemistry , pathology , immune system , disease , oxidative stress , biochemistry , in vitro , cd8
We have attempted to investigate the relative roles of specific cytotoxic T lymphocytes (CTL) and allospecific suppressor T cells (T 5 ) in the systemic and intestinal manifestations of acute graft‐versus‐host reaction (GvHR) in mice. Treatment adult (C57Bl/10xDBA/2)F 1 (BDF 1 ) mice with the suppressor cell‐specific toxin 2'‐deoxyguanosine (dGuo) inhibited the weight loss and mortality which normally occur after induction of GvHR and C57BI donor cells. dGuo also delayed the development of a destructive enteropathy as typified by jejunal villus atrophy. Paradoxically, dGuo completely prevented villus atrophy during an acute GvHR in neonatal (CBA × BALB/c)F 1 hosts, despite having only a slight ability to inhibit the systemic disease. In both models. dGuo had no effect on the generation of splenomegaly or anti‐host CTL. and dGuo‐treated mice with GvHR actually had increased proliferative alterations in the intestine, as assessed by crypt hyperplasia, In parallel. dGuo prevented the loss of NK cells which normally occurs in acute GvHR. Thus dGuo inhibits many of the destructive features of systemic and intestinal GvHR without affecting the development of CTL. We conclude that a dGuo‐sensitive mechanism causes the transition from a proliferative to a destructive GvHR.