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CD98hc facilitates B cell proliferation and adaptive humoral immunity.

  • Author(s): Cantor, Joseph;
  • Browne, Cecille D;
  • Ruppert, Raphael;
  • Féral, Chloé C;
  • Fässler, Reinhard;
  • Rickert, Robert C;
  • Ginsberg, Mark H
  • et al.

Published Web Location

https://doi.org/10.1038/ni.1712
Abstract

The proliferation of antigen-specific lymphocytes and resulting clonal expansion are essential for adaptive immunity. We report here that B cell-specific deletion of the heavy chain of CD98 (CD98hc) resulted in lower antibody responses due to total suppression of B cell proliferation and subsequent plasma cell formation. Deletion of CD98hc did not impair early B cell activation but did inhibit later activation of the mitogen-activated protein kinase Erk1/2 and downregulation of the cell cycle inhibitor p27. Reconstitution of CD98hc-deficient B cells with CD98hc mutants showed that the integrin-binding domain of CD98hc was required for B cell proliferation but that the amino acid-transport function of CD98hc was dispensable for this. Thus, CD98hc supports integrin-dependent rapid proliferation of B cells. We propose that the advantage of adaptive immunity favored the appearance of CD98hc in vertebrates.

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