Autoantibodies and B Cells in Takayasu Arteritis and Giant Cell Arteritis: Comparative Insights into Large-Vessel Vasculitis

Large-vessel vasculitis (LVV) encompasses Takayasu arteritis (TAK) and giant cell arteritis (GCA), both characterized by granulomatous inflammation of large arteries. While these diseases have distinct clinical features, the emergence of large-vessel GCA (LV-GCA) highlights an area of overlap with late-onset TAK. Although T cell- and macrophage-driven inflammation represents a shared hallmark, the contribution of B cells and autoantibodies remains less clearly defined. This review comparatively summarizes B cell mediated responses and autoantibody involvement in TAK and GCA. TAK demonstrates significant B cell activity, evidenced by B cell infiltration and the presence of tertiary lymphoid organs (TLOs) within the arterial wall. Importantly, specific autoantibodies, such as anti-endothelial protein C receptor (EPCR) and anti-scavenger receptor class B type I antibodies, have been identified. Anti-EPCR antibodies specifically associate TAK with coexisting ulcerative colitis, suggesting a shared aberrant immune pathway. In contrast, cranial GCA is primarily T cell-driven and contains relatively few B cells. However, aortic lesions in LV-GCA exhibit extensive B cell and plasma cell infiltration, including TLOs, indicating that this subtype shares key B cell mediated responses with TAK. Despite this immunological convergence, the specific autoantibody profiles appear distinct and remain incompletely characterized. Taken together, B cell and autoantibody responses are more pronounced and functionally relevant in TAK, show intermediate involvement in LV-GCA, and are least prominent in cranial GCA. These differences provide critical insights for LVV subtyping and underscore the need for further elucidation of the pathomechanisms underlying TAK, late-onset TAK, LV-GCA, and cranial GCA to enable personalized therapeutic strategies.