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      Cell-autonomous and -non-autonomous roles of CTLA-4 in immune regulation.

      Trends in Immunology
      Animals, Antibodies, Neutralizing, pharmacology, Antigen-Presenting Cells, cytology, immunology, metabolism, Antigens, CD80, Antigens, CD86, Autoimmune Diseases, pathology, therapy, CTLA-4 Antigen, antagonists & inhibitors, deficiency, genetics, Cell Communication, Forkhead Transcription Factors, Homeostasis, Immune Tolerance, drug effects, Immunity, Immunotherapy, methods, Lymphocyte Activation, Mice, Mice, Knockout, Signal Transduction, T-Lymphocytes, Regulatory

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          Abstract

          It is controversial how cytotoxic T lymphocyte antigen (CTLA)-4, a co-inhibitory molecule, contributes to immunological tolerance and negative control of immune responses. Its role as an inducer of cell-intrinsic negative signals to activated effector T cells is well documented. However, there is accumulating evidence that CTLA-4 is essential for the function of naturally occurring Foxp3(+) regulatory T (Treg) cells, which constitutively express the molecule. CTLA-4 deficiency in Foxp3(+) Treg cells indeed impairs their in vivo and in vitro suppressive function. Further, Treg cells can modulate the function of CD80- and CD86-expressing antigen-presenting cells via CTLA-4. Here we discuss how CTLA-4 expression by one T cell can influence the activation of another in a cell non-autonomous fashion and thus control immune responses. Copyright © 2011 Elsevier Ltd. All rights reserved.

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