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TACI-Ig neutralizes molecules critical for B cell development and autoimmune disease. impaired B cell maturation in mice lacking BLyS.

Immunity | Aug 24, 2001

http://www.ncbi.nlm.nih.gov/pubmed/11520463

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.

Pubmed ID: 11520463 RIS Download

Mesh terms: Animals | Antibody Formation | Arthritis, Rheumatoid | Autoantibodies | Autoimmune Diseases | B-Cell Activation Factor Receptor | B-Lymphocytes | Cell Differentiation | Cell Lineage | Collagen | Homozygote | Immunoglobulins | Membrane Proteins | Mice | Mice, Transgenic | Phenotype | Receptors, Tumor Necrosis Factor | Transmembrane Activator and CAML Interactor Protein

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