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Fig. 1 | Arthritis Research & Therapy

Fig. 1

From: Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells

Fig. 1

Cigarette smoke exposure induces arthritis aggravation in an IL-17RA-dependent manner. a AIA mice were exposed to cigarette smoke during immunization (none, one, two or three cigarettes on days 12 and 17 after immunization). Numbers of neutrophils in the joints and articular hyperalgesia was determined. b CIA mice were exposed to cigarette smoke (two cigarettes/day) or forced air alone (days 12 and 17 after immunization). Arthritis incidence and clinical scores were recorded up to day 30 (two-way ANOVA followed by Bonferroni post hoc test; n = 10, air exposed; n = 10, cigarette smoke). Numbers of neutrophils in the joint was quantified by MPO activity. Mean ± SEM, n = 10, air exposed; n = 9, cigarette smoke. *P < 0.05, **P < 0.01, ***P < 0.001 (two-sided Student’s t test). c Il17a mRNA expression in DLNs of AIA mice was determined 19 days after the first immunization (as in b). Mean ± SEM, n = 5/group. *P < 0.05, **P < 0.001, one-way ANOVA followed by Bonferroni post hoc test. d Th17 frequency in DLNs of AIA mice. Mean ± SEM, n = 4/group, *P < 0.05, one-way ANOVA followed by Bonferroni post hoc test. e AIA in WT or Il17ra−/− mice exposed to cigarette smoke or air (as in b). Mean ± SEM, n = 5/group, ***P < 0.001, one-way-ANOVA followed by Bonferroni post hoc test. All data are representative of two independent experiments. DLN draining lymph nodes, IL-17 interleukin 17, MPO myeloperoxidase

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