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. Author manuscript; available in PMC: 2012 Jun 1.
Published in final edited form as: Arthritis Rheum. 2011 Jun;63(6):1603–1612. doi: 10.1002/art.30271

Figure 1. JNK1 is critical for effector function in AIA.

Figure 1

A) Representative H&E and Safranin O stained sections of knee joints on day 10 of AIA induction in WT and JNK-deficient mice (n=14–16/group). Original magnification 200x. B) Sections above were scored for inflammatory infiltration, bone erosion and cartilage damage. Jnk1−/− mice had significantly lower scores than WT and Jnk2−/− mice. Results are expressed as means ± SEM.* p< 0.05 vs. WT and Jnk2−/− mice. C) RNA samples from whole joints (6 mice/group) were analyzed by qPCR in triplicate for expression of the indicated genes. mRNA amounts were normalized to 18S rRNA and fold induction is relative to PBS-injected joints of the same genotype. Induction of cytokine and MMP3 expression was less in Jnk1−/− mice. Results are expressed as means ± SEM.* p< 0.05 vs. WT and Jnk2−/− mice.