In addition, we used calreticulin as an adjuvant, and others have demonstrated that calreticulin increases CD8 T cell responses. In conclusion, our current data demonstrate that adenoviral vectors expressing fusion proteins consisting of CRT and ESAT-6 promote a specific immune response but do not protect against TB challenge. SCEG received a PhD scholarship from the National Council of Science and Technology (CONACYT) of México. This work was supported in part by a grant to RMDOL from PAICYT, UANL and CONACYT of PLX4032 price México. Funding for the mouse studies research was provided by

NIH, NIAID NO1-AI-40091. “
“An adequate effector response against pathogens and its subsequent inactivation after pathogen clearance are critical for the maintenance of immune homeostasis. This process involves an initial phase of T-cell effector (Teff) activation followed by the expansion of regulatory T cells selleck kinase inhibitor (Tregs), a unique cell population that limits Teff functions. However, significant questions remain unanswered about the mechanisms that regulate the balance between these cell populations. Using an in vitro system to mimic T-cell activation in human peripheral blood mononuclear cells (PBMC), we analysed the patterns of Treg and Teff activation, with special attention

to the role of type I interferon (IFN-I). Interestingly, we found that IFN-α, either exogenously added or endogenously induced, suppressed the generation of CD4+ FoxP3HI IFN-γNeg activated Tregs (aTregs) while simultaneously promoting propagation of CD4+ FoxP3Low/Neg IFN-γPos activated Teffs (aTeffs). We also showed that IFN-α-mediated inhibition of interleukin (IL)-2 production may play an essential role in IFN-α-induced

suppression of aTregs. In order to test our findings in a disease state with chronically elevated IFN-α, we investigated systemic lupus erythematosus (SLE). Plasma from patients with SLE was found to contain IFN-I activity that suppressed aTreg generation. Furthermore, anti-CD3 activated SLE PBMCs exhibited preferential expansion of aTeffs with a very limited increase in aTreg numbers. Tideglusib Together, these observations support a model whereby a transient production of IFN-α (such as is seen in an early antiviral response) may promote CD4 effector functions by delaying aTreg generation, but a chronic elevation of IFN-α may tip the aTeff:aTreg balance towards aTeffs and autoimmunity. Regulatory T cells (Tregs) are a distinct thymically derived or inducible subset of T cells with unique abilities to suppress immune responses and to maintain immunological unresponsiveness to self-antigens.1 The absence of Tregs in knock-out or antibody depletion mouse models leads to systemic autoimmunity.