Injections of an agonistic CLEC5A Ab (together with arthritis-inducing Ab mix) in the above model further increased the myeloid cell infiltration into the joint and aggravated disease severity, while the functional blockade of the CLEC5A receptor via gene deletion or injection of CLEC5A-Fc reduced the clinical signs of murine arthritis [4]. The gene discussed is CLEC5A; the disease is Arthritis.