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Immunobiology. 2014 Sep;219(9):671-9. doi: 10.1016/j.imbio.2014.03.018. Epub 2014 Apr 8.

Expression and regulation of complement receptors by human natural killer cells.

Author information

1
Core Research Laboratory, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
2
Core Research Laboratory, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China; The Fifth Hospital of Xi'an, China.
3
Core Research Laboratory, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China; Department of General Surgery, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
4
Medical Research Council (MRC) Centre for Transplantation, King's College London, Guy's Hospital, London, UK.

Abstract

Integration of cellular and humoral arms of the innate immune response is fundamental to the development of powerful effector functions in host defence as well as aberrant immune responses. Here, we provide evidence in support of the relationship between complement activation and NK cell functional modulation. We demonstrate that human NK cells and both CD56(bright)CD16(-) and CD56(dim)CD16(+) populations express receptors known to detect the biologically active peptides C3a and C5a (i.e. C3aR, C5aR, C5L2) and the covalently-bound fragments C3b and metabolites iC3b and C3d which serve in immune adhesion (e.g. CR3, CR4). We also show that several pathogen- or tumour/inflammation-related stimuli differentially regulated those complement receptor expression. Furthermore, our results suggest that C3 fragments (C3a, iC3b) have a negative regulatory effect on IFN-γ production in NK cells. This work provides extensive information of human complement receptors relevant to the integrated actions of complement and NK cells which has been suggested by animal studies. The observations may act as a resource that allows further understanding and exploitation of role of complement in human health and immune mediated diseases.

KEYWORDS:

Complement receptors; NK cells; Receptor expression; Subsets of NK cells

PMID:
24775270
DOI:
10.1016/j.imbio.2014.03.018
[Indexed for MEDLINE]
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