Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Type

Journal article

Journal

J Immunol

Publication Date

01/08/1999

Volume

163

Pages

1128 - 1131

Keywords

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