CCL21 attenuates HSV-induced inflammation through up-regulation of CD8+ memory cells.

Abstract

CCR7 and its ligand, CCL21, are known to establish microenvironments for the initiation of immune responses in secondary lymphoid tissue. It has also been reported that CCR7 ligand gene-deleted mice have defects in lymphocyte homing. In addition, the injection of the CCR7 ligand was shown to induce the expression of memory T cells. In this study, we analyzed the expression of CCR7 and its ligand in HSV-induced Behçet's disease (BD)-like inflammation of mice. Additionally, plasmids containing the CCR7 ligand CCL19 or CCL21, pcDNA3.1-CCL19 or pcDNA3.1-CCL21, respectively, were injected into symptomatic mice, and changes in the population of memory T cells were determined. After administration of pcDNA3.1-CCL21, the frequencies of CD8+CD44+, CD8+CD62L- memory T cells were significantly up-regulated and the symptoms were not deteriorated when compared to the control vector injected group. Specifically, the difference in frequencies of CCR7+ peripheral blood mononuclear cells between active BD patients and inactive BD patients was similar to that of HSV-induced BD-like mice. These results suggest that CCR7, its ligand, and CD8+ memory cells are correlated with the regulation of BD symptoms.