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

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.
Authors	J A Gross, S R Dillon, S Mudri, J Johnston, A Littau, R Roque, M Rixon, O Schou, K P Foley, H Haugen, S McMillen, K Waggie, R W Schreckhise, K Shoemaker, T Vu, M Moore, A Grossman, C H Clegg
Journal	Immunity (Immunity) Vol. 15 Issue 2 Pg. 289-302 (Aug 2001) ISSN: 1074-7613 [Print] United States
PMID	11520463 (Publication Type: Journal Article)
Chemical References	Autoantibodies B-Cell Activation Factor Receptor BLyS receptor Immunoglobulins Membrane Proteins Receptors, Tumor Necrosis Factor Tnfrsf13b protein, mouse Tnfrsf13c protein, mouse Transmembrane Activator and CAML Interactor Protein Collagen
Topics	Animals Antibody Formation Arthritis, Rheumatoid (etiology, immunology) Autoantibodies (blood) Autoimmune Diseases (etiology) B-Cell Activation Factor Receptor B-Lymphocytes (classification, immunology) Cell Differentiation Cell Lineage Collagen (immunology) Homozygote Immunoglobulins (blood) Membrane Proteins Mice Mice, Transgenic Phenotype Receptors, Tumor Necrosis Factor (genetics, immunology, metabolism) Transmembrane Activator and CAML Interactor Protein

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