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CTLA-4 is a critical negative regulator of T cell responses and CTLA-4-deficient (CTLA-4(-/-)) mice die of a lymphproliferative disease. Nevertheless, RAG-2-deficient mice reconstituted with a mixture of CTLA-4(-/-) and normal (CTLA-4(+/+)) bone marrow survive in the absence of any signs of disease, although 50% of their T cells do not express CTLA-4. Using such mixed chimeras, we analyzed the role of CTLA-4 in specific T cell responses to lymphocytic choriomeningitis virus, Leishmania major and mouse mammary tumor virus, which cause acute, chronic and persistent infections, respectively. The populations of antigen-specific CTLA-4(-/-)CD4(+) and CTLA-4(-/-)CD8(+) T cells became activated, expanded and contracted indistinguishably from CTLA-4(+/+)CD4(+) and CTLA-4(+/+)CD8(+) T cells after infection with all three pathogens. Thus, CTLA-4 is not involved in the down-regulation of specific T cell responses and peripheral deletion in a T cell-autonomous fashion.

Original publication

DOI

10.1002/1521-4141(200102)31:2<450::aid-immu450>3.0.co;2-x

Type

Journal article

Journal

Eur J Immunol

Publication Date

02/2001

Volume

31

Pages

450 - 458

Keywords

Abatacept, Animals, Antigens, CD, Antigens, Differentiation, CTLA-4 Antigen, Chimera, Cytokines, Immunoconjugates, Leishmania major, Lymphocyte Count, Lymphocytic choriomeningitis virus, Mammary Tumor Virus, Mouse, Mice, T-Lymphocytes, Th1 Cells