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Abstract
In the immune system, many tolerance checkpoints exist to prevent self-antigens from
stimulating the relentless growth of self-reactive B and T lymphocytes. The genes
and molecular pathways underpinning these checkpoints overlap with those involved
in tumor suppression. As with an inherited predisposition to cancer, inherited defects
in self-tolerance genes typically precipitate autoimmune disease stochastically after
a latent phase. Multiple mutations, inherited and somatic, may be needed before a
self-reactive clone bypasses sequential tolerance checkpoints resulting in the emergence
of autoimmune disease.