Abstract
B7 delivers a costimulatory signal through CD28, resulting in interleukin-2 secretion and T cell proliferation. Blockade of this pathway results in T cell anergy. The in vivo role of B7 was evaluated with B7-deficient mice. These mice had a 70 percent decrease in costimulation of the response to alloantigen. Despite lacking B7 expression, activated B cells from these mice bound CTLA-4 and GL1 monoclonal antibody, demonstrating that alternative CTLA-4 ligand or ligands exist. These receptors are functionally important because the residual allogenic mixed lymphocyte responses were blocked by CTLA4Ig. Characterization of these CTLA-4 ligands should lead to strategies for manipulating the immune response.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Abatacept
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Animals
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Antigens, CD
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Antigens, Differentiation / immunology
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Antigens, Differentiation / metabolism*
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B-Lymphocytes / immunology*
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B7-1 Antigen / genetics
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B7-1 Antigen / immunology*
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B7-1 Antigen / metabolism
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Base Sequence
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CTLA-4 Antigen
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Cell Line
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Immunoconjugates*
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Interleukin-2 / metabolism
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Isoantigens / immunology
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Lymphocyte Activation
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Lymphocyte Culture Test, Mixed
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Mice, Knockout
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Molecular Sequence Data
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Mutation
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T-Lymphocytes / immunology*
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Transfection
Substances
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Antigens, CD
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Antigens, Differentiation
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B7-1 Antigen
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CTLA-4 Antigen
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Ctla4 protein, mouse
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Immunoconjugates
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Interleukin-2
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Isoantigens
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Abatacept