Analyses of phenotypic and functional characteristics of CX3CR1-expressing natural killer cells

Tools

Item Type:	Article
Title:	Analyses of phenotypic and functional characteristics of CX3CR1-expressing natural killer cells
Creators Name:	Hamann, I., Unterwalder, N., Cardona, A.E., Meisel, C., Zipp, F., Ransohoff, R.M. and Infante-Duarte, C.
Abstract:	Summary We previously demonstrated a correlation between the frequency of CX3CR1-expressing human natural killer (NK) cells and disease activity in multiple sclerosis and showed that CX3CR1(high) NK cells were more cytotoxic than their CX3CR1(neg/low) counterparts. Here we aimed to determine whether human NK cell fractions defined by CX3CR1 represent distinct subtypes. Phenotypic and functional NK cell analyses revealed that, distinct from CX3CR1(high) , CX3CR1(neg/low) NK cells expressed high amounts of type 2 cytokines, proliferated robustly in response to interleukin-2 and promoted a strong up-regulation of the key co-stimulatory molecule CD40 on monocytes. Co-expression analyses of CX3CR1 and CD56 demonstrated the existence of different NK cell fractions based on the surface expression of these two surface markers, the CX3CR1(neg) CD56(bright) , CX3CR1(neg) CD56(dim) and CX3CR1(high) CD56(dim) fractions. Additional investigations on the expression of NK cell receptors (KIR, NKG2A, NKp30 and NKp46) and the maturation markers CD27, CD62L and CD57 indicated that CX3CR1 expression of CD56(dim) discriminated between an intermediary CX3CR1(neg) CD56(dim) and fully mature CX3CR1(high) CD56(dim) NK cell fractions. Hence, CX3CR1 emerges as an additional differentiation marker that may link NK cell maturation with the ability to migrate to different organs including the central nervous system.
Keywords:	Chemokines, CX3CR1, Natural Killer Cell Maturation, Natural Killer Cell Phenotypes, Natural Killer Cells
Source:	Immunology
ISSN:	0019-2805
Publisher:	Wiley-Blackwell
Volume:	133
Number:	1
Page Range:	62-73
Date:	May 2011
Official Publication:	https://doi.org/10.1111/j.1365-2567.2011.03409.x
PubMed:	View item in PubMed

Repository Staff Only: item control page