CTLA-4 ligation delivers a unique signal to resting human CD4 T cells that inhibits interleukin-2 secretion but allows Bcl-X(L) induction

J Immunol. 1998 Jan 1;160(1):12-5.

Abstract

We have assessed the functional effects of a panel of CTLA-4 mAbs on resting human CD4+ T cells. Our results demonstrate that some CTLA-4 mAbs can inhibit proliferative responses of resting CD4+ cells and cell cycle transition from G0 to G1. The inhibitory effects of CTLA-4 were evident within 4 h, at a time when cell surface CTLA-4 expression remained undetectable. Other CTLA-4 mAbs had no detectable inhibitory effects, indicating that binding of Ab to CTLA-4 alone is not sufficient to mediate down-regulation of T cell responses. Interestingly, while IL-2 production was shut off, inhibitory anti-CTLA-4 mAbs permitted induction and expression of the cell survival gene bcl-X(L). Consistent with this observation, cells remained viable and apoptosis was not detected after CTLA-4 ligation.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Abatacept
  • Antibodies, Monoclonal
  • Antigens, CD
  • Antigens, Differentiation / physiology*
  • CD4-Positive T-Lymphocytes / physiology*
  • CTLA-4 Antigen
  • Cell Cycle
  • Cells, Cultured
  • Gene Expression
  • Humans
  • Immunoconjugates*
  • Interleukin-2 / metabolism*
  • Lymphocyte Activation
  • Proto-Oncogene Proteins c-bcl-2 / physiology*
  • RNA, Messenger / genetics
  • Signal Transduction
  • bcl-X Protein

Substances

  • Antibodies, Monoclonal
  • Antigens, CD
  • Antigens, Differentiation
  • BCL2L1 protein, human
  • CTLA-4 Antigen
  • CTLA4 protein, human
  • Immunoconjugates
  • Interleukin-2
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • bcl-X Protein
  • Abatacept