Together the data demonstrate a linkage of TLR and BCR-signaling during B-1 cell responses to infections, with intrinsic TLR-mediated signaling triggering a rapid reorganization of the IgM-BCR-signalosome complex, including the removal of the BCR-signaling inhibitor CD5 and increased association of IgM-BCR with the co-receptor CD19, and the TLR-dependent differentiation of CD5+ B-1 to CD5- IgM-secreting B-1 and B-1PC. The gene discussed is BCR; the disease is infection.