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Clin Immunol. 2010 Feb;134(2):158-68. doi: 10.1016/j.clim.2009.10.001. Epub 2009 Nov 1.

NK cell activation by KIR-binding antibody 1-7F9 and response to HIV-infected autologous cells in viremic and controller HIV-infected patients.

Author information

1
Department of Microbiology, Tumor and Cell Biology and Strategic Research Center IRIS, Karolinska Institutet, Stockholm, Sweden. Susanne.Johansson@smi.se

Abstract

Natural killer (NK) cells may be protective in HIV infection and are inhibited by killer cell immunoglobulin-like receptors (KIRs) interacting with MHC class I molecules, including HLA-C. Retention of HLA-C despite downregulation of other MHC class I molecules on HIV infected cells might protect infected cells from NK cell recognition in vitro. To assess the role of inhibitory HLA-C ligands in the capacity of NK cells to recognize autologous infected T cells, we measured NK cell degranulation in vitro in viremic patients, controllers with low viremia, and healthy donors. No difference in NK cell response to uninfected compared to HIV-1(IIIB) infected targets was observed. Activation of NK cells was regulated by KIRs, because NK cell degranulation was increased by 1-7F9, a human antibody that binds KIR2DL1/L2/L3 and KIR2DS1/S2, and this effect was most pronounced in KIR haplotype B individuals.

PMID:
19880352
DOI:
10.1016/j.clim.2009.10.001
[Indexed for MEDLINE]

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