Figure 5: Neutrophil-specific CARD9 deletion attenuates autoantibody-induced inflammation.
(a,b) CARD9 expression was detected by western blot in cell-sorted bone marrow-derived neutrophils (a) or cultured macrophages (b) of wild type, Card9−/− or Card9ΔPMN animals. (c,d) Wild type (WT), Card9−/− or Card9ΔPMN bone marrow chimeras were injected with B × N (control) or K/B × N (arthritic) serum i.p. on day 0. Arthritis development was followed by clinical scoring of the hind limbs (c) and ankle-thickness measurement (d). Blistering skin disease was triggered in wild type (WT), Card9−/− or Card9ΔPMN intact mice or bone marrow chimeras by systemic injection of collagen VII-specific (anti-CVII) antibodies. Skin disease was followed by clinical assessment of the total body surface affected (e) and the overall disease severity (f). The blots are representative of three to four independent experiments. Quantitative data show mean and s.e.m. from 7 control and 8 to 9 arthritic serum-treated individual mice per group from three independent experiments (c,d) or 3 to 4 control and 4 anti-CVII-treated mice per group from two independent experiments (e,f). *P<0.05 (two-way ANOVA); NS, not significant; see the text for actual P values.
