Our experimental data show that articular AdipoR1 knockdown reduces IgG production in the knee joints of CIA mice, suggesting that local AD may stimulate B cell activation and differentiation into IgG-secreting plasma cells in the knee joint to produce anti-collagen antibodies, which may represent a mechanism by which AD drives B-cell response in addition to its recognized function in promoting T-cell response, leading to aggravated arthritis progression during the pathogenesis of CIA. The gene discussed is ADIPOR1; the disease is Alzheimer disease.