Abstract
Leukotriene B4 receptor 1 (BLT1) triggers the migration of granulocytes and activated T cells; however, its role in B-cell function remains unclear. Here we report that BLT1 is required to induce the production of antigen-specific IgA against oral vaccine through mediating innate immune signals from commensal bacteria. B cells acquire BLT1 expression during their differentiation to IgA+ B cells and plasma cells in Peyer’s patches and the small intestinal lamina propria, respectively. BLT1 KO mice exhibited impaired production of antigen-specific fecal IgA to oral vaccine despite normal IgG responses to systemically immunized antigen. Expression of MyD88 was decreased in BLT1 KO gut B cells and consequently led to diminished proliferation of commensal bacteria-dependent plasma cells. These results indicate that BLT1 enhances the proliferation of commensal bacteria-dependent IgA+ plasma cells through the induction of MyD88 and thereby plays a key role in the production of antigen-specific intestinal IgA.
Highlights
Leukotriene B4 receptor 1 (BLT1) is a G-protein-coupled highaffinity receptor for leukotriene B4 (LTB4), a metabolite of arachidonic acid.[1]
The expression of Blt[1] mRNA in splenic B cells was scant to nonexistent (Supplementary Fig. S3). These findings suggest that the cell surface expression of BLT1 in intestinal IgA+ B cells is induced at the transcriptional level
Our results suggest that BLT1 signaling enhanced the microbe-dependent proliferation of DISCUSSION In this study, we showed that BLT1 expression was required for full activation of antigen-specific IgA production against oral vaccine
Summary
Leukotriene B4 receptor 1 (BLT1) is a G-protein-coupled highaffinity receptor for leukotriene B4 (LTB4), a metabolite of arachidonic acid.[1] BLT1 is expressed on various types of immune cells, including activated T cells such as Th1 and Th2 cells,[2] CD8+ effector T cells,[3,4] and Th17 cells;[5] mast cell progenitor cells;[6] macrophages;[7] dendritic cells;[8] eosinophils;[9] and neutrophils.[10,11]. The activation of BLT1 by LTB4 primarily induces the Gαi-mediated signaling pathway, which induces cell migration to inflamed tissues where LTB4 is highly concentrated.[12,13] In addition, BLT1mediated signals enhance the FcγR-dependent phagocytic activity of macrophages,[7] and IL-12 production by dendritic cells.[8]. BLT1 is expressed on B cells in human peripheral blood and bone marrow,[19,20] and LTB4 enhances B-cell proliferation and IgG and IgM production in vitro.[21,22] little information is available regarding the role of LTB4–BLT1 signaling in B cells in vivo
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