Genetic dissection of SLE: Sle1 and FAS impact alternate pathways leading to lymphoproliferative autoimmunity

Journal of Experimental Medicine

Volumn 196, Issue 3, 2002, Pages 281-292

  Shi, Xiaoyan ^a   Xie, Chun ^a   Kreska, Desi ^a   Richardson, James A ^a   Mohan, Chandra ^a  

^a UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER   (United States)

Author keywords

ALPS; Anti DNA; Apoptosis; Genetics; Lupus

Indexed keywords

ANTINUCLEAR ANTIBODY; AUTOANTIBODY; DNA ANTIBODY; FAS ANTIGEN; GENE PRODUCT; GLOMERULUS BASEMENT MEMBRANE ANTIBODY; HISTONE ANTIBODY; IMMUNOGLOBULIN G; IMMUNOGLOBULIN G ANTIBODY; IMMUNOGLOBULIN M; PROTEIN SLE1; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; AUTOIMMUNE DISEASE; CLINICAL EXAMINATION; CONTROLLED STUDY; GENE DOSAGE; GENE LOCUS; GLOMERULONEPHRITIS; HISTOPATHOLOGY; LUPUS ERYTHEMATOSUS NEPHRITIS; LYMPHOPROLIFERATIVE DISEASE; MORTALITY; NONHUMAN; PATHOGENESIS; PHENOTYPE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PROTEIN INTERACTION; RECESSIVE GENE; SEROLOGY; SYSTEMIC LUPUS ERYTHEMATOSUS;

ANIMALS; ANTIBODIES, ANTINUCLEAR; AUTOANTIBODIES; AUTOIMMUNE DISEASES; CD4-CD8 RATIO; CELLS, CULTURED; CHROMOSOME MAPPING; GENE DOSAGE; GLOMERULONEPHRITIS; IMMUNOGLOBULIN G; LUPUS ERYTHEMATOSUS, SYSTEMIC; LYMPHOPROLIFERATIVE DISORDERS; MICE; MICE, INBRED C57BL; MICE, INBRED MRL LPR; SPLENOMEGALY;

EID: 0037025942     PISSN: 00221007     EISSN: None     Source Type: Journal    
DOI: 10.1084/jem.20010955     Document Type: Article

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