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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.


Journal article


Journal of immunology (Baltimore, Md. : 1950)

Publication Date





1128 - 1131


Basel Institute for Immunology, Switzerland.


Liver, Pericardium, T-Lymphocyte Subsets, CD4-Positive T-Lymphocytes, Bone Marrow Cells, Animals, Mice, Congenic, Mice, Inbred C57BL, Radiation Chimera, Mice, Knockout, Mice, Lymphoproliferative Disorders, Antigens, Differentiation, Antigens, CD, Immunoconjugates, Bone Marrow Transplantation, Lymphocyte Activation, Cell Movement, CTLA-4 Antigen