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β1-Adrenergic receptor autoantibodies are associated with deleterious consequences; however, the IgG3 subclass provides beneficial outcomes in human heart failure. IgG3 β1AR autoantibody inhibits G-protein coupling, simultaneously activating ERK through G-protein–independent arrestin-dependent mechanisms.

The IgG3 subclass of β1-adrenergic receptor autoantibodies is an endogenous biaser of β1AR signaling