December 6, 1999 | Fabienne Mackay, Stephen A. Woodcock, Pornsri Lawton, Christine Ambrose, Manfred Baetscher, Pascal Schneider, Jurg Tschoopp, Jeffrey L. Browning
Mice transgenic for BAFF (B cell activating factor belonging to the TNF family) develop autoimmune-like disorders, including high levels of rheumatoid factors, circulating immune complexes, anti-DNA autoantibodies, and immunoglobulin deposition in the kidneys. These mice exhibit increased numbers of mature B and effector T cells, along with signs of B cell activation and T cell alterations. BAFF, a TNF family member, binds to B cells and promotes their growth. Transgenic mice overexpressing BAFF under a liver-specific promoter show expanded B cell compartments, increased Ig levels, and autoimmune manifestations. The study highlights the role of BAFF in B cell regulation and its potential involvement in autoimmune diseases. BAFF overexpression leads to the expansion of B cells, increased Ig production, and autoimmune-like symptoms, suggesting that dysregulation of BAFF expression may contribute to autoimmunity. The findings provide insights into the mechanisms underlying autoimmune disorders and suggest that BAFF could be a target for therapeutic interventions.Mice transgenic for BAFF (B cell activating factor belonging to the TNF family) develop autoimmune-like disorders, including high levels of rheumatoid factors, circulating immune complexes, anti-DNA autoantibodies, and immunoglobulin deposition in the kidneys. These mice exhibit increased numbers of mature B and effector T cells, along with signs of B cell activation and T cell alterations. BAFF, a TNF family member, binds to B cells and promotes their growth. Transgenic mice overexpressing BAFF under a liver-specific promoter show expanded B cell compartments, increased Ig levels, and autoimmune manifestations. The study highlights the role of BAFF in B cell regulation and its potential involvement in autoimmune diseases. BAFF overexpression leads to the expansion of B cells, increased Ig production, and autoimmune-like symptoms, suggesting that dysregulation of BAFF expression may contribute to autoimmunity. The findings provide insights into the mechanisms underlying autoimmune disorders and suggest that BAFF could be a target for therapeutic interventions.