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Abstract
BackgroundMemory B cells are an antigen-experienced B-cell population with the ability to rapidly differentiate into antibody-producing cells by recall responses. We recently found that dedicator of cytokinesis 11 (DOCK11) contributes to the expansion of antigen-specific populations among germinal center B cells upon immunization. In comparison, limited information is available on the contribution of DOCK11 to secondary humoral immune responses.ResultsIn this study, effects of the DOCK11 deficiency in B cells were examined on secondary immune responses to protein antigen. The lack of DOCK11 in B cells resulted in the impaired induction of antibody-producing cells upon secondary immunization with protein antigen. DOCK11 was dispensable for the recall responses of antigen-experienced B cells, as demonstrated by the comparable induction of antibody-producing cells in mice given transfer of antigen-experienced B cells with no DOCK11 expression. Instead, the lack of DOCK11 in B cells resulted in the impaired secondary immune responses in a B cell-extrinsic manner, which was recovered by the adoptive transfer of cognate T cells.ConclusionsWe addressed that intrinsic and extrinsic effects of DOCK11 expression in B cells may contribute to secondary humoral immune responses in manner of the induction of cognate T-cell help.
Highlights
Memory B cells are an antigen-experienced B-cell population with the ability to rapidly differentiate into antibody-producing cells by recall responses
Impact of the dedicator of cytokinesis 11 (DOCK11) deficiency in B cells on secondary immune responses To examine the impact of the DOCK11 deficiency in B cells on the secondary immune responses, Dock11fl mice [10] were crossed with Cd19-Cre mice [12]
Only 2.6 times the number of NP-specific immunoglobulin G1 (IgG1)-producing cells were induced by secondary immunization of DOCK11-deficient mice
Summary
Memory B cells are an antigen-experienced B-cell population with the ability to rapidly differentiate into antibody-producing cells by recall responses. Immunological memory formation against new antigens is impaired with age, which results in limited responses to vaccination in the elderly. We successively demonstrated that DOCK11 was associated with bone marrow B cell development and marginal zone B cell formation [10] In addition to this function, we recently found that DOCK11 potentially contributes to the expansion of antigen-specific populations among GC B cells upon immunization [11]. In contrast, antibody production upon secondary immunization was impaired when the conditional knockout mice were used as recipients, indicating DOCK11 expression by B cells may contribute to the recall reaction by B cell-extrinsic manner
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