Combined with these results, our findings suggest that Helios plays important roles in immature B lymphocytes through cooperation with other

Ikaros family proteins. Tanespimycin However, more accurate functions of Helios in immature B lymphocytes should be elucidated in the future, because there are some serious problems caused by both levels and complexities of expressions of Ikaros family proteins including Helios and their various isoforms. Albeit, our results, together with previous results, may significantly help in the understanding of the B lymphocyte-specific mechanisms of PKC gene expressions and molecular mechanisms of the BCR-mediated apoptosis involved in negative selection as in auto-immune diseases and leukemias/lymphomas. This work was supported in part by Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan. We thank H. Madhyastha and R. Madhyastha for editorial reading of the

manuscript. “
“Pathogens that colonize the same or different organs can interact via cytokine-mediated pathways. Cytokines can modulate immune responses both at the local site of infection and systemically through bystander effects, and by doing so play a key role in facilitating communication between organs, constituent tissues and ultimately influencing the establishment and survival of pathogens that infect Sunitinib supplier these organs [1] and [2]. Pathogen specific cytokine responses lead to different cytokine signals, however, similar groups of pathogens often show similar profiles such as the clearly identified mutual inhibition between IFN-γ and IL-4 in the control of bacterial/viral and helminth

infections, respectively, [3]. For instance, the liver fluke Fasciola hepatica caused up-regulation of IL-4 expression and down-regulation of IFN-γ against Bordetella pertussis, resulting in delayed bacterial clearance from the lower Glycogen branching enzyme respiratory tract [4]. However, this may be far from universal. In the Trichuris muris–Schistosoma mansoni mouse model, where T. muris is restricted to the intestine and S. mansoni migrates through different organs during the parasitic life cycle, T. muris was associated with increased IL-10 and suppression of protective IFN-γ and IL-4 in the lungs, but not the liver [5]. This facilitated increased survival and migration of S. mansoni larvae from the lungs to the liver, where they developed into adults and caused augmented pathology. More recently, it has been suggested that systemic cytokine effects are influenced by inherent differences in the structure, function and immune conditioning of the infected organ, rather than being simply driven by pathogen specific responses [6], [7], [8], [9] and [10].