ecific antibody-secreting cells in bone marrow and persisting vaccine-specific serum antibodies. Our study sheds light on the mechanisms behind the adjuvanticity of LT-K63 and identifies molecular pathways that should be triggered by vaccine adjuvants to induce sustained humoral immunity in early life. Chagas disease caused by ( ) affects approximately six million individuals worldwide. Clinical manifestations are expected to occur due to the parasite persistence and host immune response. Herein we investigated potential associations between , , , or polymorphism profiles and cardiomyopathy or parasitemia, as well as the impact of HIV infection on cardiopathy. Two hundred twenty-six patients and 90 control individuals were analyzed. rs1143627 T>C, rs1800795 C>G, rs2275913 G>A, rs187238 C>G, and rs1946518 C>A SNVs were analyzed by real-time PCR and parasitemia by PCR. Our data revealed association between a cytokine gene polymorphism and parasitemia never previously reported. The rs1800795 CG genotype lowered the risk of positive parasitemia (OR=0.45, 95% CI 0.24-0.86, P=0.015). Original findings included associations between rs2275913 AA and s1946518 AA genotypes with decreased risk of developing cardiomyopathy (OR=0.27, 95% CI 0.07-0.97, P=0.0udies.Tumor immunity is a rapidly evolving area of research consisting of many possible permutations of immune cell tumor interactions that are dependent upon cell type, tumor type, and stage in tumor progression. At the same time, the majority of cancer immunotherapies have been focused on modulating the T cell-mediated antitumor immune response and have largely ignored the potential utility that B cells possess with respect to tumor immunity. Therefore, this motivated an exploration into the role that B cells and their accompanying chemokine, CXCL13, play in tumor immunity across multiple tumor types. Both B cells and CXCL13 possess dualistic impacts on tumor progression and tumor immunity which is furthered detail in this review. Specifically, various B cells subtypes are able to suppress or enhance several important immunological functions. Paradoxically, CXCL13 has been shown to drive several pro-growth and invasive signaling pathways across multiple tumor types, while also, correlating with improved survival and immune cell tumor localization in other tumor types. Potential tools for better elucidating the mechanisms by which B cells and CXCL13 impact the antitumor immune response are also discussed. In addition, multiples strategies are proposed for modulating the B cell-CXCL13 axis for cancer immunotherapies.Myeloid cells are critical cells involved in the orchestration of innate and adaptive immune responses. Most myeloid cells derive from the adult bone marrow in a process called myelopoiesis, a tightly controlled process that ensures constant production of myeloid cells. Sex differences in myeloid cell development have been observed; males exhibit greater monocytic differentiation in the bone marrow, and men have increased blood monocyte numbers when compared to women. Here we use a genetic mouse model of myeloid androgen receptor (AR) knockout (MARKO) and pharmacological inhibition of AR to investigate the role of androgen signaling in monocytic differentiation. We observe that although myeloid AR signaling does not influence total bone marrow cell numbers, it does affect the composition of the bone marrow myeloid population in both homeostatic and emergency settings. Genetic deletion of AR in myeloid cells led to reduced monocytic development in vivo. Similarly, pharmacologic inhibition of AR signaling in vitro reduced monocytic development. However, alteration in monocytic differentiation in the absence of AR signaling did not lead to reduced numbers of circulating myeloid cells, although MARKO male mice display reduced ratio of classical to non-classical monocytes in the blood, implying that blood monocyte subsets are skewed upon myeloid AR deletion. Our results suggest that the sex differences observed in monocytic differentiation are partly attributed to the positive role of the androgen-AR axis in regulating monocytic development directly at the myeloid cell level. Furthermore, we have identified a novel role for AR in regulating blood mature monocyte subset turnover. Investigating how androgen signaling affects monocytic development and monocyte subset heterogeneity will advance our understanding of sex differences in monocytic function at homeostasis and disease and can ultimately impact future therapeutic design targeting monocytes in the clinic.The intestinal microbiota constitutes a complex ecosystem in constant reciprocal interactions with the immune, neuroendocrine, and neural systems of the host. CC-930 Recent molecular technological advances allow for the exploration of this living organ and better facilitates our understanding of the biological importance of intestinal microbes in health and disease. Clinical and experimental studies demonstrate that intestinal microbes may be intimately involved in the progression of diseases of the central nervous system (CNS), including those of affective and psychiatric nature. Gut microbes regulate neuroinflammatory processes, play a role in balancing the concentrations of neurotransmitters and could provide beneficial effects against neurodegeneration. In this review, we explore some of these reciprocal interactions between gut microbes and the CNS during experimental disease and suggest that therapeutic approaches impacting the gut-brain axis may represent the next avenue for the treatment of psychiatric disorders.Influenza A viruses (IAVs) circulate widely among different mammalian and avian hosts and sometimes give rise to zoonotic infections. Vaccination is a mainstay of IAV prevention and control. However, the efficacy of IAV vaccines is often suboptimal because of insufficient cross-protection among different IAV genotypes and subtypes as well as the inability to keep up with the rapid molecular evolution of IAV strains. Much attention is focused on improving IAV vaccine efficiency using adjuvants, which are substances that can modulate and enhance immune responses to co-administered antigens. The current review is focused on a non-traditional approach of adjuvanting IAV vaccines by therapeutically targeting the immunomodulatory functions of a rare population of innate-like T lymphocytes called invariant natural killer T (iNKT) cells. These cells bridge the innate and adaptive immune systems and are capable of stimulating a wide array of immune cells that enhance vaccine-mediated immune responses. Here we discuss the factors that influence the adjuvant effects of iNKT cells for influenza vaccines as well as the obstacles that must be overcome before this novel adjuvant approach can be considered for human or veterinary use.