Genetic dissection of SLE pathogenesis. Sle1 on murine chromosome 1 leads to a selective loss of tolerance to H2A/H2B/DNA subnucleosomes.
about
Caspase-activated DNase is required for maintenance of tolerance to lupus nuclear autoantigensThe genetics of rheumatoid arthritis and the need for animal models to find and understand the underlying genesDefects in Germinal Center Selection in SLELinking susceptibility genes and pathogenesis mechanisms using mouse models of systemic lupus erythematosusA polymorphism in a phosphotyrosine signalling motif of CD229 (Ly9, SLAMF3) alters SH2 domain binding and T-cell activationImmune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosusBreaking tolerance to double stranded DNA, nucleosome, and other nuclear antigens is not required for the pathogenesis of lupus glomerulonephritis.Cgnz1 allele confers kidney resistance to damage preventing progression of immune complex-mediated acute lupus glomerulonephritis.Development of murine lupus involves the combined genetic contribution of the SLAM and FcgammaR intervals within the Nba2 autoimmune susceptibility locus.Genetic approach to study lupus glomerulonephritis.Auto-antibody production and glomerulonephritis in congenic Slamf1-/- and Slamf2-/- [B6.129] but not in Slamf1-/- and Slamf2-/- [BALB/c.129] mice.The lupus-prone NZM2410/NZW strain-derived Sle1b sublocus alters the germinal center checkpoint in female mice in a B cell-intrinsic manner.The lupus susceptibility locus Sle3 is not sufficient to accelerate atherosclerosis in lupus-susceptible low density lipoprotein receptor-deficient mice.Daily Moderate Exercise Is Beneficial and Social Stress Is Detrimental to Disease Pathology in Murine Lupus NephritisDefective B-cell response to T-dependent immunization in lupus-prone miceNew Zealand mixed mice: a genetic systemic lupus erythematosus model for assessing environmental effects.PARP alleles within the linked chromosomal region are associated with systemic lupus erythematosusGenetic dissection of lupus pathogenesis: a recipe for nephrophilic autoantibodies.What causes alopecia areata?The lupus susceptibility locus Sle1 breaches peripheral B cell tolerance at the antibody-forming cell and germinal center checkpointsExpansion of immunoglobulin-secreting cells and defects in B cell tolerance in Rag-dependent immunodeficiency.Activation of rheumatoid factor-specific B cells is antigen dependent and occurs preferentially outside of germinal centers in the lupus-prone NZM2410 mouse modelDysregulated cytokine production by dendritic cells modulates B cell responses in the NZM2410 mouse model of lupusGerminal center B cell depletion diminishes CD4+ follicular T helper cells in autoimmune miceThe major murine systemic lupus erythematosus susceptibility locus, Sle1, is a cluster of functionally related genes.CXCR4/CXCL12 hyperexpression plays a pivotal role in the pathogenesis of lupus.Murine lupus susceptibility locus Sle1a requires the expression of two sub-loci to induce inflammatory T cellsYaa autoimmune phenotypes are conferred by overexpression of TLR7.B cell-intrinsic TLR7 signaling is essential for the development of spontaneous germinal centers.Murine models of systemic lupus erythematosusLatent membrane protein 1, the EBV-encoded oncogenic mimic of CD40, accelerates autoimmunity in B6.Sle1 miceSusceptibility genes in the pathogenesis of murine lupus.A Tlr7 translocation accelerates systemic autoimmunity in murine lupus.An allelic variant of Crry in the murine Sle1c lupus susceptibility interval is not impaired in its ability to regulate complement activation.Murine lupus susceptibility locus Sle2 activates DNA-reactive B cells through two sub-loci with distinct phenotypesCutting edge: an NK cell-independent role for Slamf4 in controlling humoral autoimmunity.A New Zealand Black-derived locus suppresses chronic graft-versus-host disease and autoantibody production through nonlymphoid bone marrow-derived cellsA novel isoform of the Ly108 gene ameliorates murine lupus.Anti-dsDNA antibodies and disease classification in antinuclear antibody positive patients: the role of analytical diversity.Oxidative stress as a potential causal factor for autoimmune hemolytic anemia and systemic lupus erythematosus
P2860
Q24626603-2A22FFA7-0595-4F05-A44E-0F0E450F58B7Q24805318-D7BCE062-5A6B-4C76-8EB3-DCC15FA3904FQ26796041-E6ECAC3C-8ACA-4F90-8FFC-44B1E61D21EBQ26822662-765DB9A4-F91B-40B7-8D35-EC5987EE322DQ28115070-FC2BA5DE-D687-4D10-9447-D75F170F566EQ28591255-5165F380-4AA2-4FC2-8ADD-03C90BC706FCQ30312212-3633D988-1BB0-42B1-8225-547473158F60Q30413753-AF729B00-52AC-4519-BB9C-58C62273DE76Q30433488-A8D08469-B7B6-4290-B7F1-9422F59E8811Q30456024-E882CDB0-6681-4CDA-9FB5-9B1CB36A5E40Q30500838-66DEC48B-6DA1-429D-9185-3D802B51F16BQ30529641-DDA86D8E-AEB2-418C-91A2-D764AE80BA1EQ33575750-3FA74D96-1D1D-472D-B0D7-EA83D29EAC66Q33603442-BC414FB5-85CB-442F-9EE6-AC27033C6A38Q33689667-D07D54DB-004B-449A-87A2-C75385231A2EQ33741182-1C0286FC-D6B2-493A-9169-CC1379B05DF7Q33849511-D112F002-084D-43A8-BF49-C5DDD61A29FEQ33853007-FBD053DA-236D-4DEE-A19C-F345DA601A76Q33889367-DACD96DF-B1A6-405E-A887-55B4A7B55B8DQ33890686-7AA56C91-CC6C-43B2-8275-71E18EF22509Q33979850-7BC3BB3B-ED61-4224-ACA5-5859FF87A7A6Q33992536-BCDB293E-E054-41BF-9F28-8CE6DA6B00A0Q34004649-36CC48F2-F0A4-438C-814D-3DA01F551A4AQ34015403-4D020C98-CEB8-4422-90F2-2EACDA8F125CQ34104677-D1163D64-9ED2-4F5B-82D9-774B90F47A39Q34157254-276ED252-8901-4C48-AA44-5213722A0AB7Q34217717-D08C289C-A695-4CE7-BE3F-3F3CF50E3E8BQ34356566-E20ED349-DFD4-4DEF-8ED6-960E3A98D309Q34364711-C1892B18-B649-41B8-835A-E08D11D4F44DQ34591019-37985768-4CAA-463E-9113-7B351D725CBAQ34622693-2502F942-5B01-43D0-B91B-A6E088DB0ED7Q34731237-9E767798-A33A-49FC-B016-14C8E4101A71Q34773105-7C04FB2A-A3C6-4AD7-8552-7BA8C557DA2AQ34775999-9E875CFC-4D75-4071-B0C3-760E30A676CDQ34842443-D7E18975-D93F-4D6A-B4A2-5AC3257EFB58Q35058871-D8534708-041D-42B0-9210-AFFE49787AECQ35092315-1B032E23-D923-4DE5-98C8-410D03056328Q35102250-59940F1A-C9D9-4550-80DB-89683350AEB4Q35553962-27D44608-201F-462D-8848-B55E93125AF7Q35567857-948AA5DF-0B7B-41C2-95CC-82F0B607C648
P2860
Genetic dissection of SLE pathogenesis. Sle1 on murine chromosome 1 leads to a selective loss of tolerance to H2A/H2B/DNA subnucleosomes.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on March 1998
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Genetic dissection of SLE path ...... to H2A/H2B/DNA subnucleosomes.
@en
Genetic dissection of SLE path ...... to H2A/H2B/DNA subnucleosomes.
@nl
type
label
Genetic dissection of SLE path ...... to H2A/H2B/DNA subnucleosomes.
@en
Genetic dissection of SLE path ...... to H2A/H2B/DNA subnucleosomes.
@nl
prefLabel
Genetic dissection of SLE path ...... to H2A/H2B/DNA subnucleosomes.
@en
Genetic dissection of SLE path ...... to H2A/H2B/DNA subnucleosomes.
@nl
P2093
P2860
P1476
Genetic dissection of SLE path ...... to H2A/H2B/DNA subnucleosomes.
@en
P2093
P2860
P304
P407
P577
1998-03-01T00:00:00Z