To prevent autoimmunity, it is critical that tolerance mechanisms block autoantibody
production from self-reactive B cells. B cell tolerance is maintained through mechanisms
that can reversibly or irreversibly silence autoreactive B cells. Of these mechanisms, those
that lead to B cell death offer the most reliable form of tolerance to prevent autoimmunity. In
many cases, death of autoreactive B cells is regulated by the cell intrinsic, or mitochondrial
pathway of cell death. The pro-apoptotic Bcl-2 family proteins, Bak, Bax, and Bim have been
shown to be required for disruption of mitochondria and intrinsic cell death of self-reactive B
cells whereas the anti-apoptotic Bcl-2, Bcl-xL, and Mcl-1 can prevent cell death by interfering
with the action of Bax and Bak. Bcl-2 and Bcl-xL have also been shown to regulate
the autophagic cell death pathway that may also play a role in B cell tolerance. Even after
mitochondrial disruption, mechanisms exist that may impede activation of caspases and
death of autoreactive B cells. Together, understanding of cell death mechanisms and how
they may affect B cell tolerance has made significant recent advances and it is now important
to incorporate alternate and post-mitochondrial cell death mechanisms into B cell tolerance
Copyright / Drug Dosage
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