Previous studies have shown that CD1dhiCD5+ B cells, transitional 2-marginal zone precursors (T2-MZP; CD23hiCD21hiIgM+), antibody-secreting cells (CD44hiCD138+ plasmablasts), and peritoneal CD5+ B1a cells can, through the production of IL-10, suppress pathogenic T cells and inhibit autoimmune inflammatory diseases such as experimental autoimmune encephalomyelitis (EAE), arthritis, and colitis, as well as contact hypersensitivity7–10. Here, IL10 is linked to arthritic joint disease.