Cutting Edge: Expression of Chemokine Receptor CXCR1 on Human Effector CD8+ T Cells

Abstract

IL-8 is a potent inflammatory cytokine that induces chemotaxis of neutrophils expressing CXCR1 and CXCR2, thus indicating its involvement in the migration of these cells to inflammatory sites where bacteria proliferate. Presently, we showed that CXCR1+ cells were predominantly found among CD8+ T cells having effector phenotype, and that the expression of CXCR1 was positively correlated with that of perforin, suggesting that CXCR1 is expressed on effector CD8+ T cells. Indeed, human CMV-specific CD8+ T cells from healthy individuals, which mostly express the effector phenotype and have cytolytic function, expressed CXCR1, whereas EBV-specific CD8+ T cells, which mostly express the memory phenotype and have no cytolytic function, did not express this receptor. The results of a chemotaxis assay showed that the migration of CXCR1+CD8+ T cells was induced by IL-8. These results suggest that the IL-8-CXCR1 pathway plays an important role in the homing of effector CD8+ T cells.

Down‐regulation of CXCR4 expression on human CD8+ T cells during peripheral differentiation

“…Our recent study demonstrated that the surface expression of CXCR1 is positively correlated with that of perforin [24]. These findings suggest that the expression of CXCR4 correlates negatively with the expression of CXCR1.…”

“…CD27 -CD28 -CD45RA - [7,15,23]. A recent study demonstrated that CXCR1 is expressed on effector and effector/memory CD8 + T cells with phenotypes of CD27 -CD28 -CD45RA +/-and CD27 low CD28 -CD45RA +/-, respectively, and that the expression of CXCR1 correlates with that of perforin [24].…”

IL‐15‐induced human DC efficiently prime melanoma‐specific naive CD8+ T cells to differentiate into CTL

“…Indeed, recent studies have identified a subset of human CD8 + T cells that express CXCR1, respond to IL-8 and have cytotoxic function [22,23]. Memory CD8 + T cells do not express this receptor [22,23].…”

Properties of murine CD8+CD27- T cells

“…In uninfected mice the mean percentage of CD27 -cells within the lung CD8 + T-cell population was 11% and upon influenza infection this increased to 20% at day 9 and 29% at day 20 after infection ( Table 1). The increase in the lung at day 9 was possibly due to nonspecific migration of CD8 + CD27 -memory T cells in response to inflammatory mediators produced in inflamed lung [38][39][40] because at this time point nearly Liver 208 Table 2. In a CD27 x CD62L dot plot three subpopulations were identified: R1, CD62L + CD27 + ; R2, CD62L -CD27 + ; R3, CD62L -CD27 -.…”