IL17A and arthritic joint disease: However, previously, our work has demonstrated that the helminth product ES-62 disrupts the IL-17 network in arthritis models without promoting a Th2 phenotype: rather, by resetting homeostatic regulatory mechanisms (regulatory B cell and IL-22-dependent synovial fibroblast tissue repair responses), ES-62 acts to interfere with a number of the key pathological processes required to drive inflammation and disease (14, 17, 22, 35).