The benefit of such deactivation is to decrease the instances of aberrant immune responses, such as allergic and autoimmune disorders. Pathogenic microorganisms may also have evolved to express antigens that cross-react with gut flora antigens. In infections, the removal or modification of the gut flora is associated with a modification of the phenotype of the host responses. Therefore, some microorganisms may hijack Tregs that are induced or activated

in the gut to limit pathogenic check details responses against gut flora to ensure their own survival. Over time, established GI infections may create a new homeostatic set point, in which reactivity to the chronic pathogen is minimized, with wider implications for responsiveness selleck antibody to self-antigens and allergens which may not be altogether detrimental. At this point, it remains unclear to what extent any recalibration of host immunity is induced purely by the pathogen, or by perturbation of the commensal population, or is a result

of endogenous controls within the immune system itself. On the basis of both human and experimental studies discussed above, it seems likely that all three components play an essential role in reaching a stable and nonpathogenic steady state for the longer term. None. “
“Pregnancy challenges immune cells and immunomodulatory circuits of the mother and the developing fetus to dynamically adapt to each other in an homeostatic and tolerant environment Org 27569 for fetal growth. This entails the coordination of multiple cellular processes all devoted to accommodate and nourish the fetus while protecting the mother from endogenous and exogenous threatens. From the earliest stages of pregnancy, several strategies to efficiently

communicate immune and trophoblast cells within the interface or at a distance were identified and chemokines might act at on different targets through direct or indirect mechanisms. Here, we briefly review some mechanisms of T regulatory cell recruitment to the early maternal–placental interfaces to accomplish immunotolerance and homeostatic control and we discuss evidence on two locally released polypeptides, RANTES (regulated on activation, normal, T-cell expressed, and secreted) and vasoactive intestinal peptide (VIP), as novel contributors to the multiplicity of immune tolerant responses and uterine quiescence requirements.