Variations in expression and/or function of a number of genes confer increased risk of development of autoimmunity. Among these variations is the expression negative regulators of the PI3K pathway, whose activity is critical in maintaining B cell anergy or unresponsiveness. Acute deletion of SHIP-1 or PTEN in autoreactive B cells leads to autoimmunity. The Cambier lab reports the ability to pharmacologically correct defects in PI3K pathway regulation which confer risk of autoimmunity, thus preventing autoimmunity while conferring minimal disruption of adaptive immune function. PI3K inhibitors can be used therapeutically to compensate for decreased negative regulation of the PI3K pathway. This technology has the potential to aid in the development of precision treatments for autoimmunity that act by correcting effects of specific risk alleles.
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