Abstract
The molecular mechanisms why mutations of the lipopolysaccharide-responsive beige-like anchor (LRBA) paradoxically cause both autoimmunity and common variable immunodeficiency (CVID) are unknown. LRBA regulates vesicle trafficking and signal transduction required for the regulation and function of many immune molecules. It is hypothesized that LRBA deficiency attenuates both activation and deactivation of nuclear factor kappa beta (NFkB) resulting in immunodeficiency and autoimmunity.
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