Fas (CD95) induces macrophage proinflammatory chemokine production via a MyD88-dependent, caspase-independent pathway

Journal of Leukocyte Biology

Volumn 82, Issue 3, 2007, Pages 721-728

  Altemeier, William A ^a,c   Zhu, Xiaodong ^a   Berrington, William R ^a   Harlan, John M ^a   Liles, W Conrad ^a,b  

^a UNIVERSITY OF WASHINGTON SCHOOL OF MEDICINE   (United States)

^b UNIVERSITY OF TORONTO   (Canada)

^c UNIVERSITY OF WASHINGTON   (United States)

Author keywords

Apoptosis; Inflammation; Lung injury; Neutrophil

Indexed keywords

CASPASE; CHEMOKINE; CXCL1 CHEMOKINE; FAS ANTIGEN; INTERLEUKIN 1 RECEPTOR; MYELOID DIFFERENTIATION FACTOR 88;

ANIMAL CELL; ANIMAL EXPERIMENT; APOPTOSIS; ARTICLE; CONTROLLED STUDY; HYPOTHESIS; IN VIVO STUDY; LEUKOCYTE; MACROPHAGE; MOUSE; NEUTROPHIL; NONHUMAN; POLYMORPHONUCLEAR CELL; PRIORITY JOURNAL; PROTEIN EXPRESSION; UPREGULATION;

ANIMALS; ANTIBODIES, MONOCLONAL; ANTIGENS, CD95; APOPTOSIS; CASPASES; CHEMOKINES; CHEMOKINES, CXC; FEMALE; MACROPHAGES; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MYELOID DIFFERENTIATION FACTOR 88; RECEPTORS, INTERLEUKIN-1; RNA, SMALL INTERFERING; SERPINS; SIGNAL TRANSDUCTION; VIRAL PROTEINS;

MUS;

EID: 34548383501     PISSN: 07415400     EISSN: None     Source Type: Journal    
DOI: 10.1189/jlb.1006652     Document Type: Article

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