In particular, numerous endogenous products derived from necrotic cells including nucleic acids, high-mobility group protein B1 (HMGB1), heat shock proteins (HSPs) as well as nucleic acid antigen-autoantibody formed immune complexes are involved in B cell overactivation via TLRs and activate T cell-independent antibody response in lupus development [13,14,15]. Here, HMGB1 is linked to systemic lupus erythematosus.