Polyautoimmunity, the coexistence of two or more autoimmune diseases in the same individual, often reflects shared genetic, environmental, and immunological mechanisms. A key immunological link between Rheumatoid Arthritis (RA) and autoimmune thyroid diseases (AITDs)—such as Hashimoto’s thyroiditis and Graves’ disease—is the central involvement of B cells. Traditionally recognized for antibody production, B cells also function as antigen-presenting cells (APCs), cytokine producers, and regulators of T-cell responses. These diverse roles position them as crucial contributors to the initiation and perpetuation of multi-organ autoimmunity. In RA, B cells promote joint inflammation by generating autoantibodies such as rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPAs), presenting arthritogenic antigens, and producing proinflammatory cytokines like IL-6 and TNF-α. In thyroid autoimmunity, B cells drive disease through the production of thyroid-directed autoantibodies (TPOAb, TgAb, and TSHR-stimulating antibodies), contributing to thyroid gland dysfunction and chronic inflammation.