Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6020579 | Journal of Neuroimmunology | 2014 | 4 Pages |
â¢CD98 is required on B cells for efficient induction of MOG-induced EAE.â¢Loss of B cell CD98 blocks autoantibody production after immunization with MOG.â¢Targeting CD98 does not appear to affect steady-state B cell functions.â¢CD98 is a potential therapeutic target in the antibody-dependent subset of MS.
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.