caa a22 4500 467906769 CHVBK 20180406152836.0 cr unu---uuuuu 170328e20060201xx s 000 0 eng 10.1007/s00251-005-0066-1 doi (NATIONALLICENCE)springer-10.1007/s00251-005-0066-1 Genetic control of anti-Sm autoantibody production in NOD congenic mice narrowed to the Idd9.3 region [Elektronische Daten] [Junichiro Irie, Yuehong Wu, David Sass, William Ridgway] Anti-Smith (anti-Sm) autoantibodies are directed to proteins in the small-nuclear ribonucleoprotein (snRNP) family and are considered specific for systemic lupus erythematosus (SLE) in both humans and mice. We previously established that NOD.c3c4 mice, carrying B6 and B10 congenic segments from chromosomes 3 to 4 on an nonobese diabetic (NOD) background, and NOD.Idd9R28 mice, carrying a B10 segment on c4 alone, developed significant penetrance of anti-Sm antibody production. Here we determine autoantibody incidence in additional NOD.Idd9 congenic strains and use a congenic mapping approach to narrow the interval necessary for enhanced autoantibody production to a ∼5.6-Mb region containing insulin-dependent diabetes (Idd)9.3. The Idd9.3 interval contains the candidate molecule cluster of differentiation (CD)137, which is a member of the tumor necrosis factor (TNF) receptor superfamily, functions as an inducible costimulator of T cells, and controls T-B interactions. The NOD and B10 CD137 alleles have sequence polymorphisms and different functional effects on T cells; the NOD CD137 allele mediates weaker T cell proliferative responses and decreased interleukin (IL)-2 production after CD137-mediated costimulation. Our work establishes CD137 as a candidate gene for control of autoantibody production in NOD.Idd9.3 congenic mice. Springer-Verlag, 2006 CD137 nationallicence Autoantibodies nationallicence Anti-Sm antibodies nationallicence SLE nationallicence Nonobese diabetic mouse nationallicence Congenic mice nationallicence Irie Junichiro Division of Rheumatology and Immunology, University of Pittsburgh School of Medicine, 15261, Pittsburgh, PA, USA aut Wu Yuehong Division of Rheumatology and Immunology, University of Pittsburgh School of Medicine, 15261, Pittsburgh, PA, USA aut Sass David Division of Rheumatology and Immunology, University of Pittsburgh School of Medicine, 15261, Pittsburgh, PA, USA aut Ridgway William Division of Rheumatology and Immunology, University of Pittsburgh School of Medicine, 15261, Pittsburgh, PA, USA aut Immunogenetics Springer-Verlag 58/1(2006-02-01), 9-14 0093-7711 58:1<9 2006 58 251 https://doi.org/10.1007/s00251-005-0066-1 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00251-005-0066-1 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Irie Junichiro Division of Rheumatology and Immunology, University of Pittsburgh School of Medicine, 15261, Pittsburgh, PA, USA aut NATIONALLICENCE 700 1- Wu Yuehong Division of Rheumatology and Immunology, University of Pittsburgh School of Medicine, 15261, Pittsburgh, PA, USA aut NATIONALLICENCE 700 1- Sass David Division of Rheumatology and Immunology, University of Pittsburgh School of Medicine, 15261, Pittsburgh, PA, USA aut NATIONALLICENCE 700 1- Ridgway William Division of Rheumatology and Immunology, University of Pittsburgh School of Medicine, 15261, Pittsburgh, PA, USA aut NATIONALLICENCE 773 0- Immunogenetics Springer-Verlag 58/1(2006-02-01), 9-14 0093-7711 58:1<9 2006 58 251 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer