Genechip analysis of CD4+T cells

【Objectives】The FPR2 is a G-protein coupled receptor that potently possesses pro- and anti-inflammatory role. Although FPR2 is known to be expressed by T cells, its function in arthritic condition is unclear. We investigated the involvement of FPR2 on T cells in GPI-induced arthritis (GIA) and rheumatoid arthritis (RA). 【Methods】Fluctuated expression of FPR2 mRNA on CD4+T cells was analyzed in GIA. We sorted FPR2+ or FPR2-CD4+T cells from arthritic lymph nodes, then the mRNA expression of various markers from CD4+T cell subsets was examined. Naïve T cells were cultured favoring Th1, Th2 and Th17 cell differentiation, then the expression of FPR2 was analyzed by FACS. In humans, the expression of FPR2 on CD4+T cells from healthy subjects (HS) or patients with RA was compared. 【Results】The expression of FPR2 in CD4+T cells was upregulated in the early phase of arthritis. FPR2+ T cells had higher expression of T-bet and IFNγ than FPR2-T cells. FPR2+ T cells were frequently detected on Th1 condition but not on Th2 and Th17. The expression of FPR2 on CD4+T cells was significantly higher in RA than in HS. 【Conclusion】We identified that FPR2+T cells showed Th1 phenotype in mice and this molecule was highly detected on CD4+T cells in patients with RA, suggesting FPR2+T cells might play a crucial role in RA. To identify the highly expressed molecules on autoreactive-CD4+T cells in GPI-induced arthritis, the mRNA expression profile of splenic CD4+ T cells isolated by Magnetic–activated cell sorting (MACS) was examined by microarray in DBA/1 mice (arthritis susceptible) and C57BL/6 mice (arthritis resistant) after immunization of GPI on day7