title: 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.affiliation: Department of Immunology, 1201 Eastlake Avenue East, Seattle, WA 98102, USA. grossj@zgi.com
authors.forename: J A
authors.initials: JA
authors.lastname: Gross
authors.forename: S R
authors.initials: SR
authors.lastname: Dillon
authors.forename: S
authors.initials: S
authors.lastname: Mudri
authors.forename: J
authors.initials: J
authors.lastname: Johnston
authors.forename: A
authors.initials: A
authors.lastname: Littau
authors.forename: R
authors.initials: R
authors.lastname: Roque
authors.forename: M
authors.initials: M
authors.lastname: Rixon
authors.forename: O
authors.initials: O
authors.lastname: Schou
authors.forename: K P
authors.initials: KP
authors.lastname: Foley
authors.forename: H
authors.initials: H
authors.lastname: Haugen
authors.forename: S
authors.initials: S
authors.lastname: McMillen
authors.forename: K
authors.initials: K
authors.lastname: Waggie
authors.forename: R W
authors.initials: RW
authors.lastname: Schreckhise
authors.forename: K
authors.initials: K
authors.lastname: Shoemaker
authors.forename: T
authors.initials: T
authors.lastname: Vu
authors.forename: M
authors.initials: M
authors.lastname: Moore
authors.forename: A
authors.initials: A
authors.lastname: Grossman
authors.forename: C H
authors.initials: CH
authors.lastname: Clegg
mesh_terms: D000818:Animals; D000917:Antibody Formation; D001172:Arthritis, Rheumatoid / Q000209:etiology / Q000276:immunology; D001323:Autoantibodies / Q000097:blood; D001327:Autoimmune Diseases / Q000209:etiology*; D053265:B-Cell Activation Factor Receptor; D001402:B-Lymphocytes / Q000145:classification / Q000276:immunology*; D002454:Cell Differentiation; D019070:Cell Lineage; D003094:Collagen / Q000276:immunology; D006720:Homozygote; D007136:Immunoglobulins / Q000097:blood; D008565:Membrane Proteins; D051379:Mice; D008822:Mice, Transgenic; D010641:Phenotype; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D053303:Transmembrane Activator and CAML Interactor Protein
chemical_list: D001323:Autoantibodies; D053265:B-Cell Activation Factor Receptor; C120197:BLyS receptor; D007136:Immunoglobulins; D008565:Membrane Proteins; D018124:Receptors, Tumor Necrosis Factor; C486361:Tnfrsf13b protein, mouse; C486662:Tnfrsf13c protein, mouse; D053303:Transmembrane Activator and CAML Interactor Protein; D003094:Collagen