However, the enhanced Th17 responses alone could be responsible, and this is supported by the fact that clinical symptoms of disease are unaffected by Ackr2 deficiency in models that exclusively examine the effector arm of disease development (such as, anti-collagen antibody-induced arthritis in DBA1/j mice; EAE in C57BL/6J mice driven by transfer of MOG35–55-primed T cells26). Here, ACKR2 is linked to arthritic joint disease.