The RhoA/ROCK inhibitor, Y27632, also attenuated disease development in lupus-prone mice by diminishing T cell production of IL-17 and IL-21 [42], and it reduced serum the levels of tumor necrosis factor-α (TNF-α), IL-1β and interleukin-6 (IL-6) while increasing the levels of IL-10 [43]. Additionally, pharmacologic RhoA/ROCK inhibition reduced the production of anti-dsDNA antibody levels and the responsiveness of B cells to B-cell activating factor receptor (BAFF/ BAFFR) [38, 44], suggesting a role in the differentiation of autoantibody-producing B lymphocytes in SLE [45]. Here, IL1B is linked to systemic lupus erythematosus.