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      Lymphoproliferative disorders with early lethality in mice deficient in Ctla-4.

      Science (New York, N.Y.)
      Animals, Antigens, CD, analysis, Antigens, CD95, metabolism, Antigens, Differentiation, genetics, physiology, Apoptosis, B-Lymphocytes, immunology, CTLA-4 Antigen, Cells, Cultured, Concanavalin A, pharmacology, Female, Gamma Rays, Gene Targeting, Homeostasis, Immunoconjugates, Immunoglobulins, blood, Immunophenotyping, Lymph Nodes, pathology, Lymphocyte Activation, Lymphoproliferative Disorders, Male, Mice, Mice, Inbred C57BL, Spleen, T-Lymphocytes

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          Abstract

          The role of the cell-surface molecule CTLA-4 in the regulation of T cell activation has been controversial. Here, lymph nodes and spleens of CTLA-4-deficient mice accumulated T cell blasts with up-regulated activation markers. These blast cells also infiltrated liver, heart, lung, and pancreas tissue, and amounts of serum immunoglobulin were elevated. The mice invariably became moribund by 3 to 4 weeks of age. Although CTLA-4-deficient T cells proliferated spontaneously and strongly when stimulated through the T cell receptor, they were sensitive to cell death induced by cross-linking of the Fas receptor and by gamma irradiation. Thus, CTLA-4 acts as a negative regulator of T cell activation and is vital for the control of lymphocyte homeostasis.

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