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Highlights • Leishmania amazonensis infection induced IL-10 production by follicular B cells. • Infected Xid mice had delayed lesion growth and lower levels of IL-10 production than WT. • Infected Xid presented lower number of total follicular B cells than WT. • Infected Xid mice presented lower levels of serum IgM, IgG. IgG1, IgG2a and IgG2b antibodies. • Infected Xid exhibited similar production of IL-10 by T Cells but less by B cells. Abstract This work aims to study the immunomodulation of B lymphocytes during L. amazonensis infection. We demonstrated in this study that follicular B cells from draining lymph nodes of infected wild type BALB/c mice are the major source of IL-10 during infection. We infected BALB/Xid mice that developed smaller lesions in comparison with the control, but the parasite load obtained from the infected tissues was similar in both groups. We observed a reduction in the number of follicular B cells from BALB/Xid mice in relation to WT mice and, consequently, lower levels of IgM, IgG, IgG1, IgG2a and IgG2b in the serum of BALB/Xid when compared with wild type mice. BALB/Xid mice also presented lower levels of IL-10 in the infected footpad, draining lymph nodes and in the spleen when compared with WT infected tissues. We did not detect differences in the number of IL-10 producing CD4+ and CD8+ T cells between WT and BALB/Xid mice; however, a strong reduction of IL-10 producing follicular B cells was noted in BALB/Xid mice. When analyzed together, our data indicate that B cells are related with lesion pathogenesis through the production of antibodies and IL-10. [ABSTRACT FROM AUTHOR]