Research Article
Chemokine Receptor Expression on Normal Blood CD56+ NK-Cells Elucidates Cell Partners That Comigrate during the Innate and Adaptive Immune Responses and Identifies a Transitional NK-Cell Population
Table 5
Homeostatic and inflammatory chemokines (CK) and chemokine receptors (CKR) involved in cell mediated immune responses and their relevance for colocalization of the NK-cell subsets with other cells of the innate-dendritic cells (DC), monocytes, neutrophils, and adaptive (T cells) immune system. Colocalization of CD56+high, CD56+int, and CD56+high NK-cells with other immune cells is signaled in blue, green, and red, respectively. Black squares inside the cells indicate positive interactions of the CK and the CKR as well as the CKR expressing cells. CD56+int NK-cells are transitional NK-cells, whose properties are intermediate between those of CD56+high and CD56+low NK-cells. CD56+high and CD56+low NK-cells are both able to produce cytokines and chemokines, upon stimulation with monokines and target cell recognition, respectively. The CK produced by NK-cells (e.g., MIP-1, MIP-1, and RANTES) not only attracted proinflammatory monocytes (via CCR1 and CCR5), immature myeloid DC (via CCR1 and CCR5), Th1 cells, and CTL (via CCR5) but also activated neutrophils (via CCR1) to the sites of inflammation. The cytokines produced by the NK-cells (e.g., IFN-, TNF-) activate monocytes, DC, neutrophils, and Th1/CTL, thereby potentiating the cell mediated immune responses. For instance, activated monocytes/DC are able to produce IFN- inducible cytokines—CXCL9 (MIG), CXCL10 (IP-10), and CXCL11 (I-TAC), which recruit more CXCR3 expressing cells (CD56+high NK-cells, Th1 cells, and CTL). In addition, CXCL8 (IL-8) produced in inflamed tissues by locally resident activated cells, such as macrophages, epithelial cells, and endothelial cells, recruits neutrophils, CD56+low NK-cells, and CTL, via interaction with CXCL1 and CXCL2.
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