Human NK receptors

From the molecules to the therapy of high risk leukemias

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Natural killer cells are important players of the innate immunity. In humans, they express HLA-class I-specific inhibitory receptors including the allotypic-specific KIR and various activating receptors. In most instances, in an autologous setting NK cells do not kill self cells. In contrast, in an allogeneic setting as the haploidentical hematopoietic stem cell transplantation to cure high risk leukemias, donor-derived NK cells may express inhibitory KIR that are not engaged by the HLA-class I alleles (KIR ligands) expressed by recipient cells. Such "alloreactive" NK cells may be responsible for the eradication of leukemia blasts escaping the preparative regimen, residual host dendritic cells and T lymphocytes, thus preventing leukemia relapse, GvHD and graft rejection, respectively. These NK-mediated effects result in a sharp improvement of the estimated 5 years survival.

Original languageEnglish
Pages (from-to)1563-1567
Number of pages5
JournalFEBS Letters
Volume585
Issue number11
DOIs
Publication statusPublished - Jun 6 2011

Fingerprint

T-cells
Stem cells
Grafts
Natural Killer Cells
Leukemia
Ligands
Molecules
Hematopoietic Stem Cell Transplantation
Graft Rejection
Therapeutics
Innate Immunity
Dendritic Cells
Alleles
T-Lymphocytes
Recurrence
Survival

Keywords

  • Activating NK receptor
  • Haploidentical hematopoietic stem cell transplantation
  • High-risk leukemia
  • Killer Ig-like receptor
  • Natural killer cell

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Genetics
  • Molecular Biology
  • Structural Biology

Cite this

Human NK receptors : From the molecules to the therapy of high risk leukemias. / Moretta, Lorenzo; Locatelli, Franco; Pende, Daniela; Sivori, Simona; Falco, Michela; Bottino, Cristina; Mingari, Maria Cristina; Moretta, Alessandro.

In: FEBS Letters, Vol. 585, No. 11, 06.06.2011, p. 1563-1567.

Research output: Contribution to journalArticle

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