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Abstract: Mature B cells expressing surface IgM as B cell receptor (BCR) consist of two B-cell subpopulations, B-1 and B-2 cells that regulate innate and acquired immunity, respectively. B-1 cells become natural Ig-producing plasma cells in response to natural ligands or self-antigens. Mature B-2 cells proliferate and differentiate into Ig-producing plasma cells under the influence of T helper (Th) cells. Antigen stimulation of B-2 cells induces class switch recombination (CSR) from IgM to other isotypes that is regulated by cytokines and activation-induced cytidine deaminase (AID). IL-5 activates B cells and eosinophils and regulates the innate and acquired immune response. IL-5 stimulates innate B-1 cells and induces the homeostatic proliferation, survival and differentiation of B cells leading to increased secretion of natural antibody. IL-5Rα-deficient mice show the impaired contact sensitivity that is mediated by activated T cells and IgM antibody produced by B-1 cells. IL-5 induces AID and Blimp-1 expression in activated B-2 cells leading to μ to γ1 CSR and IgG1 production. In contrast, IL-4 does not induce μ to γ1 CSR in anti-CD38-activated B-2 cells. Intriguingly, the costimulation of anti-CD38-activated B-2 cells with 8-mercaptoguanosine and IL-4 induces μ to γ1 CSR and IgG1 production, suggesting that unidentified factor(s) is/are required together with AID to complete CSR. We will discuss the role of IL-5 in the innate immune system and disease control, particularly the regulation of contact sensitivity and chronic inflammation through B-1 cell activation and IgM production. [Copyright &y& Elsevier]

Over the years research has found an association between B lymphocytes and pathogenesis during Leishmania sp. infections. Recently we demonstrated that B-2 lymphocytes are the main producers of IL-10 during L. amazonensis infection, and that the disease severity in BALB/c mice was attributed to these IL-10-producing B-2 lymphocytes. Here, we aim to understand the role of peritoneal B-1 lymphocytes in the pathogenesis of L. amazonensis infection. We found that infection resulted in a decrease in the number of B-1a lymphocytes and increase in B-1b lymphocytes in the peritoneal cavity of WT BALB/c mice but not in B lymphocyte deficient mice (BALB/Xid) mice. In vitro interaction between B-1 lymphocytes and L. amazonensis showed that the amastigote form of the parasite was able to induce higher levels of IL-10 in B-1 lymphocytes derived from infected BALB/c mice than the promastigote. Moreover, B-1 lymphocytes derived from infected mice produced more IL-10 than B-1 lymphocytes derived from naïve mice under amastigote interaction. However, the repopulation of BALB/Xid mice with B-1 lymphocytes from WT BALB/c mice did not affect the lesion development. Together, these results suggest that although B-1 lymphocytes are able to produce IL-10 during in vitro interaction with L. amazonensis , they are not directly related to pathogenesis in vivo. [ABSTRACT FROM AUTHOR]