B cell responses are regulated by antigen acquisition, processing, and presentation to helper T cells. These functions are thought to depend on contractile activity of non-muscle myosin IIa. Here, we show that B cell-specific deletion of the myosin IIa heavy chain reduced the numbers of bone marrow B cell precursors and splenic marginal zone, peritoneal B1b, and germinal center B cells. In addition, myosin IIa-deficient follicular B cells acquired an activated phenotype and were less efficient in chemokinesis and extraction of membrane-presented antigens. Moreover, myosin IIa was indispensable for cytokinesis. Consequently, mice with myosin IIa-deficient B cells harbored reduced serum immunoglobulin levels and did not mount robust antibody responses when immunized. Altogether, these data indicate that myosin IIa is a negative regulator of B cell activation but a positive regulator of antigen acquisition from antigen-presenting cells and that myosin IIa is essential for B cell development, proliferation, and antibody responses. B cell antigen acquisition, processing, and presentation may depend on contractile activity of the actomyosin cytoskeleton. Here, Hoogeboom et al. show that non-muscle myosin IIa positively regulates B cell antigen acquisition from antigen-presenting cells in vivo. In addition, myosin IIa negatively regulates B cell activation and is required for B cell cytokinesis.
- antigen internalization
- antigen presentation
- B cell development
- B cell response
- B cell signaling
- non-muscle myosin
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
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- School of Medicine, Dentistry and Biomedical Sciences - Patrick G. Johnston Fellow
- Wellcome Wolfson Institute for Experimental Medicine