However, Annunziato et al.  showed that significant proportions of CD4+ T cells from the gut of patients with Crohn’s disease coexpressed IFN-γ and IL-17. The discrepancy between studies might be because of the differences in specific T cell subsets activating in different disease backgrounds. We identified that both IL-22- and IL-17-producing CD4+ T cells were central memory cells with a phenotype
of CD45RA−CD62L−CCR7+CD27+. Central memory LY2109761 cells were thought to be long-lived populations, able to expand extensively for an effective secondary immune response. This contrasted with the effector memory phenotype found on IFN-γ-producing CD4+ or γδ T cells, which was CD45RA−CD62L−CCR7− [42, 44]. Taken together, our results suggested that IL-22- or IL-17-producing cells in pleural fluid were long-lived populations with the potential to contribute to long-lasting protection against TB. Elucidating
the mechanisms by which these T cell subsets might control M. tuberculosis infection is the subject of ongoing research. In conclusion, our findings of M. tuberculosis-specific IFN-γ-, IL-22- and IL-17-producing cells in tubercular pleural fluid may reflect the activation of a local protective immune response. The understanding of human local immune responses to M. tuberculosis may facilitate the evaluation of the efficacy of new anti-TB vaccines. MAPK inhibitor almost Further investigations may unravel the critical targets for therapeutic intervention in chronic inflammatory diseases. This work was supported by grant 115 (No. 2008ZX10003-011); National Nature Science Foundation of China (No. 30872300) and National Key Basic Research Program
of China (973; No. 2007CB512404). The authors declare no financial or commercial conflict of interest. “
“The relative roles that ageing and lifelong cytomegalovirus (CMV) infection have in shaping naive and memory CD4+ T-cell repertoires in healthy older people is unclear. Using multiple linear regression analysis we found that age itself is a stronger predictor than CMV seropositivity for the decrease in CD45RA+ CD27+ CD4+ T cells over time. In contrast, the increase in CD45RA− CD27− and CD45RA+ CD27− CD4+ T cells is almost exclusively the result of CMV seropositivity, with age alone having no significant effect. Furthermore, the majority of the CD45RA− CD27− and CD45RA+ CD27− CD4+ T cells in CMV-seropositive donors are specific for this virus. CD45RA+ CD27− CD4+ T cells have significantly reduced CD28, interleukin-7 receptor α (IL-7Rα) and Bcl-2 expression, Akt (ser473) phosphorylation and reduced ability to survive after T-cell receptor activation compared with the other T-cell subsets in the same donors. Despite this, the CD45RA+ CD27− subset is as multifunctional as the CD45RA− CD27+ and CD45RA− CD27− CD4+ T-cell subsets, indicating that they are not an exhausted population.