1. TACI-Ig neutralizes molecules critical for B cell development and autoimmune disease. impaired B cell maturation in mice lacking BLyS.
- Author
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Gross JA, Dillon SR, Mudri S, Johnston J, Littau A, Roque R, Rixon M, Schou O, Foley KP, Haugen H, McMillen S, Waggie K, Schreckhise RW, Shoemaker K, Vu T, Moore M, Grossman A, and Clegg CH
- Subjects
- Animals, Antibody Formation, Arthritis, Rheumatoid etiology, Arthritis, Rheumatoid immunology, Autoantibodies blood, B-Cell Activation Factor Receptor, B-Lymphocytes classification, Cell Differentiation, Cell Lineage, Collagen immunology, Homozygote, Immunoglobulins blood, Mice, Mice, Transgenic, Phenotype, Receptors, Tumor Necrosis Factor genetics, Receptors, Tumor Necrosis Factor immunology, Transmembrane Activator and CAML Interactor Protein, Autoimmune Diseases etiology, B-Lymphocytes immunology, Membrane Proteins, Receptors, Tumor Necrosis Factor metabolism
- Abstract
BLyS and APRIL have similar but distinct biological roles, mediated through two known TNF receptor family members, TACI and BCMA. We show that mice treated with TACI-Ig and TACI-Ig transgenic mice have fewer transitional T2 and mature B cells and reduced levels of circulating immunoglobulin. TACI-Ig treatment inhibits both the production of collagen-specific Abs and the progression of disease in a mouse model of rheumatoid arthritis. In BLyS-deficient mice, B cell development is blocked at the transitional T1 stage such that virtually no mature B cells are present, while B-1 cell numbers are relatively normal. These findings further elucidate the roles of BLyS and APRIL in modulating B cell development and suggest that BLyS is required for the development of most but not all mature B cell populations found in the periphery.
- Published
- 2001
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