Autoimmune disease results from multiple interactive defects in apoptosis induction molecules and signaling pathways.

Behring Institute Mitteilungen

Volumn , Issue 97, 1996, Pages 200-219

  Mountz, J D ^a   Zhou, T ^a   Su, X ^a   Cheng, J ^a   Pierson, M ^a   Bluethmann, H ^a   Edwards 3rd , C K ^a  

^a UNIVERSITY OF ALABAMA AT BIRMINGHAM   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

FAS ANTIGEN; FAS LIGAND; FASL PROTEIN, MOUSE; FASLG PROTEIN, HUMAN; LYMPHOCYTE ANTIGEN RECEPTOR; MEMBRANE PROTEIN; TUMOR NECROSIS FACTOR ALPHA; TUMOR NECROSIS FACTOR RECEPTOR;

ANIMAL; APOPTOSIS; AUTOIMMUNE DISEASE; BIOLOGICAL MODEL; GENETICS; HUMAN; IMMUNOLOGY; INFLAMMATION; LYMPHOPROLIFERATIVE DISEASE; MOUSE; MOUSE MUTANT; PATHOLOGY; PHYSIOLOGY; REVIEW; SIGNAL TRANSDUCTION;

ANIMALS; ANTIGENS, CD95; APOPTOSIS; AUTOIMMUNE DISEASES; FAS LIGAND PROTEIN; HUMANS; INFLAMMATION; LYMPHOPROLIFERATIVE DISORDERS; MEMBRANE GLYCOPROTEINS; MICE; MICE, MUTANT STRAINS; MODELS, IMMUNOLOGICAL; RECEPTOR-CD3 COMPLEX, ANTIGEN, T-CELL; RECEPTORS, TUMOR NECROSIS FACTOR; SIGNAL TRANSDUCTION; TUMOR NECROSIS FACTOR-ALPHA;

EID: 0030254402     PISSN: 03010457     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Review

References (116)