In the CIA model, administration of butyrate before disease onset prevents both initiation and progression of arthritis by promoting Tfr-cell differentiation and dampening the CII-driven GC responses [49]; In contrast butyrate fails to inhibit collagen antibody-induced arthritis (CAIA) when administered after booster immunization [49], indicating that its protective effects primarily target autoantibody generation rather than immune complex–mediated inflammation. The gene discussed is TFRC; the disease is arthritic joint disease.