Lupus, a multigenic autoimmune condition in which a breakdown of tolerance results in the development of autoantibodies, leads to a variety of pathologic outcomes. Despite the heterogeneity of factors influencing disease susceptibility, we demonstrate that the partial restoration of inhibitory Fc receptor (FcgRIIB) levels on B cells in lupus-prone mouse strains is sufficient to restore tolerance and prevent autoimmunity. FcgRIIB regulates a common B cell checkpoint in genetically diverse lupus-prone mouse strains, and modest changes in its expression can result in either tolerance or autoimmunity. Therefore, increasing FcgammaRIIB levels on B cells may be an effective way to treat autoimmune diseases.
Pubmed ID: 15681388 RIS Download
Mesh terms: Animals | Antibodies, Antinuclear | Autoantibodies | B-Lymphocytes | Bone Marrow Transplantation | Chromatin | Female | Genetic Vectors | Kidney | Lung | Lupus Erythematosus, Systemic | Macrophages | Male | Mice | Mice, Inbred C57BL | Myeloid Cells | Receptors, IgG | Retroviridae | Self Tolerance | T-Lymphocytes | Transduction, Genetic
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