Modulation of Th1 Activation and Inflammation by the NF-κB Repressor Foxj1

Science

Volumn 303, Issue 5660, 2004, Pages 1017-1020

  Lin, Ling ^a   Spoor, Melanie S ^a   Gerth, Andrea J ^a   Brody, Steven L ^a   Peng, Stanford L ^a  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

GENES; MOLECULAR BIOLOGY; PROTEINS;

CELL ACTIVATION; IMMUNE RESPONSE;

IMMUNOLOGY;

FOXJ1 PROTEIN; I KAPPA B; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; REPRESSOR PROTEIN; TRANSCRIPTION FACTOR FKHR; UNCLASSIFIED DRUG;

MEDICINE;

ARTICLE; AUTOIMMUNITY; CELL PROLIFERATION; CLINICAL PATHWAY; CYTOKINE PRODUCTION; GENE EXPRESSION REGULATION; IMMUNOMODULATION; IN VIVO STUDY; INFLAMMATION; LYMPHOCYTE; LYMPHOCYTE ACTIVATION; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION; REGULATORY MECHANISM; TH1 CELL; TRANSCRIPTION INITIATION;

ANIMALS; ANTIGEN-PRESENTING CELLS; AUTOIMMUNITY; CELL DIVISION; CELL LINE; CELL LINE, TUMOR; CELL NUCLEUS; CHIMERA; CYTOPLASM; DNA-BINDING PROTEINS; FORKHEAD TRANSCRIPTION FACTORS; GENE TARGETING; HUMANS; I-KAPPA B PROTEINS; INFLAMMATION; INTERFERON TYPE II; INTERLEUKIN-2; INTERLEUKINS; LYMPHOCYTE ACTIVATION; MICE; MICE, INBRED C57BL; NF-KAPPA B; NFATC TRANSCRIPTION FACTORS; NUCLEAR PROTEINS; TH1 CELLS; TH2 CELLS; TRANS-ACTIVATION (GENETICS); TRANSCRIPTION FACTORS;

EID: 1142286333     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.1093889     Document Type: Article

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24. We are grateful to T. Kitamura for the pMX/PlatE retroviral system; R. Schreiber for the use of the ABI PRISM (Applied Biosystems, Foster City, CA) sequence detection system; M. Oukka and L. Glimcher for the NF-κB-luc construct and the 293-T cell line; M. R. Marshall for technical assistance; and J. Green, K. Murphy, A. Shaw, and W. Yokoyama for critical commentary during the preparation of the manuscript. This work was supported in part by the Siteman Cancer, Diabetes Research and Training, and the Digestive Diseases Research Core (DK52574) Centers of the Washington University School of Medicine, as well as grants from NIH (AI01803 and AI057471 to S.L.P. and HL56244 and HL63988 to S.L.B.), the Lupus Research Institute, and the Broad Medical Research Foundation. S.I.P. is supported in part by an Arthritis Investigator award from the Arthritis Foundation. S.L.B. is a recipient of a Career Investigator award from the American Lung Association.