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      CTLA-4: a negative regulator of autoimmune disease

      The Journal of Experimental Medicine

      The Rockefeller University Press

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          Abstract

          CTLA-4, a CD28 homologue expressed on activated T cells, binds with high affinity to the CD28 ligands, B7-1 (CD80) and B7-2 (CD86). This study was designed to examine the role of CTLA-4 in regulating autoimmune disease. Murine relapsing-remitting experimental autoimmune encephalomyelitis (R-EAE) is a demyelinating disease mediated by PLP139- 151-specific CD4+ T cells in SJL/J mice. Anti-CTLA-4 mAbs (or their F(ab) fragments) enhanced in vitro proliferation and pro-inflammatory cytokine production by PLP139-151-primed lymph node cells. Addition of either reagent to in vitro activation cultures potentiated the ability of T cells to adoptively transfer disease to naive recipients. In vivo administration of anti-CTLA-4 mAb to recipients of PLP139-151-specific T cells resulted in accelerated and exacerbated disease. Finally, anti- CTLA-4 treatment of mice during disease remission resulted in the exacerbation of relapses. Collectively, these results suggest that CTLA- 4 mediates the downregulation of ongoing immune responses and plays a major role in regulating autoimmunity.

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          Author and article information

          Journal
          J Exp Med
          The Journal of Experimental Medicine
          The Rockefeller University Press
          0022-1007
          1540-9538
          1 August 1996
          : 184
          : 2
          : 783-788
          Article
          96343891
          2192746
          8760834
          Categories
          Articles

          Medicine

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