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![Figure][1] Insight from Ralf KuppersAn overactive Toll-like receptor (TLR) pathway is a hallmark of several autoimmune diseases and some types of B cell lymphomas. TLR signaling is a main mediator of inflammatory signals in B cells and causes NF-κB activation, which has numerous

IRAK4 inhibition to shut down TLR signaling in autoimmunity and MyD88-dependent lymphomas