The course of antigen-induced arthritis (AIA) is not modified by treatment with a monoclonal anti-IL-36 receptor (R) antibody or in IL-36R-deficient mice. Time course of knee joint inflammation is shown in anti-IL-36R antibody-treated mice (A, upper panel) and in IL-36R knockout (KO) mice (B, left panel) with AIA. Joint inflammation was measured by external gamma counting of 99mtechnetium (Tc) accumulation on days 1, 3 and 7 after mBSA injection into the left knee. Results are expressed as the ratio of 99mTc uptake in the left arthritic knee over the right non-inflamed knee. For each time point, the mean ± standard error of the mean (SEM) of the ratios is shown for anti-IL-36R antibody (n = 7; triangles), 9B5 (rat IgG2a anti-human CD44) isotype-matched control antibody-treated mice (n = 7; gray circles), or PBS-treated mice (n = 11; open circles), wild-type (WT) C57BL/6J mice (n = 9; black line) and IL-36R-/- mice (n = 7; dashed line). (A, lower panels; B, right panel) Histological scores for synovial inflammation and cartilage degradation 8 and 14 days after intra-articular mBSA injection. Results shown represent the mean ± SEM for anti-IL-36R antibody (n = 5 on day 8, n = 6 on day 14, black columns), 9B5 isotype control (n = 3 on day 8, n = 4 on day 14, hatched columns), PBS-treated mice (n = 3 on day 8, n = 4 on day 14, open columns) (A, lower panels), WT C57BL/6J mice (n = 9 on day 8, white columns) and IL-36R-/- mice (n = 7 on day 8, black columns) (B, right panel).
Lamacchia et al. Arthritis Research & Therapy 2013 15:R38 doi:10.1186/ar4192