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CD2 is a dominant target for allogeneic responses.

Yalai Bai1, Shuang Fu, Shaun Honig

  • 1Carl C. Icahn Institute For Gene Therapy and Molecular Medicine, and the Recanati/Miller Transplantation Institute, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|August 31, 2002
PubMed
Summary
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Blocking CD2 and CD48 with antibodies significantly improves allograft survival by inhibiting T-cell responses. Blocking 2B4, however, shows limited impact on T-cell alloreactivity and graft survival.

Area of Science:

  • Immunology
  • Transplantation Immunology

Background:

  • CD2 and 2B4 (CD244) are immunoglobulin superfamily members and ligands for CD48.
  • CD2 is expressed on T, NK, B cells, and APCs; 2B4 is on NK, T cells, and monocytes, impacting NK cytotoxicity.
  • Previous studies showed anti-CD48 plus anti-CD2 mAb combination yields indefinite allograft survival.

Purpose of the Study:

  • To investigate the role of 2B4 blockade in allograft rejection.
  • To compare the efficacy of blocking CD2, CD48, and 2B4 interactions in allograft survival and T-cell responses.

Main Methods:

  • Administered monoclonal antibodies (mAbs) against CD2, CD48, or 2B4, singly or in combination, to cardiac allograft recipients.
  • Assessed the impact of mAbs on anti-CD3 mAb and alloantigen-driven T-cell proliferation and IFN-gamma production.

Related Experiment Videos

  • Utilized CD2-/- and CD48-/- T cells and antigen-presenting cells to elucidate mAb mechanisms.

    • Main Results:

    • Anti-CD2 plus anti-CD48 mAbs achieved indefinite allograft survival.
    • Anti-CD2 plus anti-2B4 mAbs prolonged graft survival, while anti-CD48 plus anti-2B4 mAbs showed no benefit over single mAbs.
    • Anti-CD2 inhibited T-cell responses; anti-CD48 had limited effect on alloantigen responses; anti-2B4 was generally ineffective alone.
    • Combinations were effective in alloantigen-driven proliferation, correlating with allograft survival outcomes.

    Conclusions:

    • CD2-CD48 blockade is highly effective in promoting allograft survival by inhibiting T-cell responses.
    • 2B4 is not a potent regulatory molecule for CD48 in alloantigen responses.
    • Blocking the 2B4-CD48 interaction is less effective than CD2-CD48 blockade in inhibiting T-cell alloreactivity.