IL23A and arthritic joint disease: In support of these observations, there have been reports associating at least some aspects of IL-23 and TNF biology in vivo in mice and in arthritis patients [22–26, 51, 52]; IL-23 and GM-CSF have also been associated at the level of expression in vivo and in the mutual control of both adaptive and innate immune models of inflammatory/autoimmune disease in mice [15, 16, 30–33, 53–56].