Cyclosporin a regulates human NK cell apoptosis induced by soluble HLA-I or by target cells

Alessandro Poggi, Maria Raffaella Zocchi

Research output: Contribution to journalArticlepeer-review


Human natural killer (NK) cells are effectors of innate immunity, capable of killing transformed or virus-infected cells and producing pro-inflammatory cytokines. Soluble molecules of HLA-I (sHLA-I), which are significantly increased in the serum of patients affected by auto-immune or infectious or neoplastic diseases, induce NK cell apoptosis interacting with its ligands, such as CD8 or the activating isoforms of members of inhibitory superfamily receptors (IRS). This cell death is accompanied by the release of large amounts of interferon-γ. NK cells can kill autologous target cells, including antigen presenting cells or infected or tumor cells, by engaging the natural cytotoxicity receptors (NCR) NKp30, or NKp44 and NKp46. Again, the binding between NCR on NK cells and their putative ligands on targets leads to NK cell apoptosis. FasL produced and secreted by NK cells is responsible for the NK cell apoptosis induced by either HLA-I receptors or NCR. Interestingly, cyclosporin A (CsA) blocks NK cell death consequent to interaction with target cells or with sHLA-I, without affecting the activation of cytolysis. This would indicate that CsA can maintain NK cell-dependent innate immunity by prolonging NK cell survival in an hostile environment in the presence of sHLA-I or target cells.

Original languageEnglish
Pages (from-to)532-536
Number of pages5
JournalAutoimmunity Reviews
Issue number8
Publication statusPublished - Nov 2005


  • CLIR
  • Cyclosporin A
  • HLA-I
  • IFN-γ
  • IRS
  • KIR
  • NK cells

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy


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