Cutting edge: lymphoproliferative disease in the absence of CTLA-4 is not T cell autonomous

MF Bachmann, G Köhler, B Ecabert… - The Journal of …, 1999 - journals.aai.org
MF Bachmann, G Köhler, B Ecabert, TW Mak, M Kopf
The Journal of Immunology, 1999journals.aai.org
Mice deficient for the expression of CTLA-4 develop a lethal lymphoproliferative syndrome
and multiorgan inflammation leading to death at about 4 wk of age. Here we show that
RAG2-deficient mice reconstituted with CTLA-4-deficient bone marrow do not develop a
lymphoproliferative syndrome despite lymphocyte infiltration mainly into pericardium and
liver. Moreover, RAG2-deficient mice reconstituted with a mixture of normal and CTLA-4-
deficient bone marrow remain healthy and do not develop any disease. Thus, the lethal …
Abstract
Mice deficient for the expression of CTLA-4 develop a lethal lymphoproliferative syndrome and multiorgan inflammation leading to death at about 4 wk of age. Here we show that RAG2-deficient mice reconstituted with CTLA-4-deficient bone marrow do not develop a lymphoproliferative syndrome despite lymphocyte infiltration mainly into pericardium and liver. Moreover, RAG2-deficient mice reconstituted with a mixture of normal and CTLA-4-deficient bone marrow remain healthy and do not develop any disease. Thus, the lethal disease observed in CTLA-4-deficient mice is not T cell autonomous and can be prevented by factors produced by normal T cells.
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