Cell-surface CD19 functions as a general rheostat for defining intrinsic and antigen
receptor-induced signaling thresholds critical for clonal expansion of the B cell pool and
humoral immunity. CD19 also governs B cell responses initiated through the CD21 receptor,
where complement C3d binding to CD21 links humoral immune responses with the innate
immune system. Alterations in this signaling pathway can predispose mice and humans to
autoantibody production and systemic autoimmunity. Transgenic mice that overexpress CD19
by 20-170% lose tolerance and generate autoantibodies. Likewise, B cells from CD21-deficient
mice overexpress CD19 by ~ 50%, which leads to autoantibody production. Autoimmune
patients with systemic sclerosis also overexpress CD19 by ~20%, which may contribute to
their intrinsic B cell abnormalities and autoantibody production. Thus, chronic B cell activation
resulting from augmented CD19 expression or signaling through the CD19 pathway may reveal
a prototype autoimmune disease susceptibility pathway in mice and humans.
Copyright / Drug Dosage
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