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Articles by R Dunn
Total Records ( 2 ) for R Dunn
  B Pollinger , G Krishnamoorthy , K Berer , H Lassmann , M. R Bosl , R Dunn , H. S Domingues , A Holz , F. C Kurschus and H. Wekerle

We describe new T cell receptor (TCR) transgenic mice (relapsing-remitting [RR] mice) carrying a TCR specific for myelin oligodendrocyte glycoprotein (MOG) peptide 92–106 in the context of I-As. Backcrossed to the SJL/J background, most RR mice spontaneously develop RR experimental autoimmune encephalomyelitis (EAE) with episodes often altering between different central nervous system tissues like the cerebellum, optic nerve, and spinal cord. Development of spontaneous EAE depends on the presence of an intact B cell compartment and on the expression of MOG autoantigen. There is no spontaneous EAE development in B cell–depleted mice or in transgenic mice lacking MOG. Transgenic T cells seem to expand MOG autoreactive B cells from the endogenous repertoire. The expanded autoreactive B cells produce autoantibodies binding to a conformational epitope on the native MOG protein while ignoring the T cell target peptide. The secreted autoantibodies are pathogenic, enhancing demyelinating EAE episodes. RR mice constitute the first spontaneous animal model for the most common form of multiple sclerosis (MS), RR MS.

  R. S Misra , G Shi , M. E Moreno Garcia , A Thankappan , M Tighe , B Mousseau , K Kusser , S Becker Herman , K. L Hudkins , R Dunn , M. R Kehry , T. S Migone , A Marshak Rothstein , M Simon , T. D Randall , C. E Alpers , D Liggitt , D. J Rawlings and F. E. Lund

Survival of mature B cells is regulated by B cell receptor and BAFFR-dependent signals. We show that B cells from mice lacking the Gq subunit of trimeric G proteins (Gnaq–/– mice) have an intrinsic survival advantage over normal B cells, even in the absence of BAFF. Gnaq–/– B cells develop normally in the bone marrow but inappropriately survive peripheral tolerance checkpoints, leading to the accumulation of transitional, marginal zone, and follicular B cells, many of which are autoreactive. Gnaq–/– chimeric mice rapidly develop arthritis as well as other manifestations of systemic autoimmune disease. Importantly, we demonstrate that the development of the autoreactive B cell compartment is the result of an intrinsic defect in Gnaq–/– B cells, resulting in the aberrant activation of the prosurvival factor Akt. Together, these data show for the first time that signaling through trimeric G proteins is critically important for maintaining control of peripheral B cell tolerance induction and repressing autoimmunity.

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