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Abstract
Abstract Lymphocyte clonal expansion mediates adaptive immunity. Here we report that CD98hc enables humoral immunity by supporting B cell clonal expansion. Deletion of B cell CD98hc in mice through conditional gene targeting did not affect B cell compartmentalization, but did result in reduced antibody responses. The mechanism of this effect did not involve interference with early signaling from antigen receptors, but instead was due to total suppression of rapid B cell proliferation, and consequent inability to form plasma cells. CD98hc can mediate both integrin signaling and amino acid transport. Reconstitution with CD98hc mutants revealed that its integrin interaction is required and its amino acid transport function is dispensable for B cell proliferation. These data establish that CD98hc enables clonal expansion of B cells, show that this function is performed by support of cell proliferation through interaction with integrins, and suggest that adaptive immunity drove appearance of CD98hc and its ability to capacitate integrin signaling.
Published Version
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