First, our sample size may not be large enough to detect an association of a gene with the some effect of RA. Our control

groups were smaller than RA groups, so the power of this study is not too high. Nevertheless, find more the analysis of polymorphisms should rely on clinically well-described group and not just on the sample size. Unfortunately in our study, only two SNPs were tested in patients with RA and control. In conclusion, these findings demonstrated that IL-17F His161Arg variant might be associated with an increased disease activity in Polish patients with RA. However, further studies associated with IL-17F expression and its genetic analysis in large RA cohorts with clinical data is warranted. “
“Whether cytokines can influence the adaptive immune response by antigen-specific γδ T cells during infections or vaccinations remains unknown. We previously demonstrated that, during BCG/M. tuberculosis (Mtb) infections, Th17-related cytokines markedly up-regulated when phosphoantigen-specific

Vγ2Vδ2 T cells expanded. In this study, we examined the involvement of Th17-related cytokines in the recall-like responses of Vγ2Vδ2 T cells following Mtb infection or vaccination against TB. Treatment with IL-17A/IL-17F or IL-22 expanded phosphoantigen HMBPP-stimulated Vγ2Vδ2 T cells from BCG-vaccinated macaques but not from naïve animals, and IL-23 induced Tamoxifen in vitro greater expansion than the other Th17-related cytokines. Consistently, Mtb infection of macaques also enhanced the ability of IL-17/IL-22 or IL-23 to expand HMBPP-stimulated Vγ2Vδ2 T cells. When evaluating IL-23 signaling as a prototype, we found that HMBPP/IL-23-expanded Vγ2Vδ2 Aldehyde dehydrogenase T cells from macaques infected with Mtb or vaccinated with BCG or Listeria ΔactA prfA*-ESAT6/Ag85B produced IL-17, IL-22, IL-2 and IFN-γ. Interestingly, HMBPP/IL-23-induced production of IFN-γ in turn facilitated IL-23-induced

expansion of HMBPP-activated Vγ2Vδ2 T cells. Furthermore, HMBPP/IL-23-induced proliferation of Vγ2Vδ2 T cells appeared to require APC contact and involve the conventional and novel protein kinase C signaling pathways. These findings suggest that Th17-related cytokines can contribute to recall-like expansion and effector function of Ag-specific γδ T cells after infection or vaccination. This article is protected by copyright. All rights reserved “
“Treg cells express high levels of the glucocorticoid-induced tumor necrosis factor-related receptor (GITR), while resting conventional T (Tconv) cells express low levels that are increased upon activation. Manipulation of GITR/GITR-Ligand (GITR-L) interactions results in enhancement of immune responses, but it remains unclear whether this enhancement is secondary to costimulation of Tconv cells or to reversal of Treg-cell-mediated suppression.