title: CD98 is a potential target for ablating B cell clonal expansion and autoantibody in multiple sclerosis.
abstract: Current B cell-directed therapies for multiple sclerosis impact multiple B cell functions. CD98hc enables B cell clonal expansion and antibody production. I probed the relative importance of autoantibody secretion vs. other B cell functions in MS and targeted CD98hc as a possible therapeutic strategy. I report that the loss of CD98hc function in B cells largely prevents autoantibody production while preserving antigen-presenting and T cell-directing capacities. Mice lacking CD98hc in B cells are protected from EAE; importantly this is overcome with autoantibody-containing plasma. Thus CD98hc blockade is a possible avenue to treat MS by inhibiting clonal expansion and autoantibody.
authors.affiliation: Department of Medicine, University of California San Diego, MC 0726, 9500 Gilman Drive, La Jolla, CA 92093-0726, United States. Electronic address: jmcantor@ucsd.edu.
authors.forename: Joseph M
authors.initials: JM
authors.lastname: Cantor
mesh_terms: D000818:Animals; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology*; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000188:drug therapy / Q000276:immunology*; D027261:Fusion Regulatory Protein-1 / Q000276:immunology*; D006801:Humans; D051379:Mice; D008817:Mice, Mutant Strains; D009103:Multiple Sclerosis / Q000188:drug therapy / Q000276:immunology*; D063308:Myelin-Oligodendrocyte Glycoprotein / Q000276:immunology / Q000494:pharmacology; D011994:Recombinant Proteins / Q000276:immunology / Q000494:pharmacology
chemical_list: D001323:Autoantibodies; D027261:Fusion Regulatory Protein-1; C571326:MOG protein, human; D063308:Myelin-Oligodendrocyte Glycoprotein; D011994:Recombinant Proteins
keywords: Autoantibody; B cell; CD98; Clonal expansion; EAE