Blockade of the ICOSL pathway ameliorates autoimmune CIA, the K/BxN spontaneous arthritis model, and the SLE (NZB/NZW) F1 mouse model, with marked reductions in disease manifestations, numbers of TFH and GC B cells, and pathogenic, class-switched, high-affinity autoantibodies (113–115). Here, ICOSLG is linked to arthritic joint disease.