NF-κB family of transcription factors: Central regulators of innate and adaptive immune functions

Clinical Microbiology Reviews

Volumn 15, Issue 3, 2002, Pages 414-429

  Caamaño, Jorge ^a   Hunter, Christopher A ^a  

^a UNIVERSITY OF PENNSYLVANIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; TRANSCRIPTION FACTOR;

APOPTOSIS; B LYMPHOCYTE ACTIVATION; HOMEOSTASIS; IMMUNOREGULATION; INFECTION; REVIEW; T LYMPHOCYTE ACTIVATION; ANIMAL; B LYMPHOCYTE; HUMAN; IMMUNOLOGY; INNATE IMMUNITY; METABOLISM; MOUSE; SIGNAL TRANSDUCTION; T LYMPHOCYTE;

ANIMALS; B-LYMPHOCYTES; HUMANS; IMMUNITY, NATURAL; INFECTION; MICE; NF-KAPPA B; SIGNAL TRANSDUCTION; T-LYMPHOCYTES;

EID: 0035983295     PISSN: 08938512     EISSN: None     Source Type: Journal    
DOI: 10.1128/CMR.15.3.414-429.2002     Document Type: Review

References (230)

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171. The role of natural killer cells in host-parasite interactions
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173. Multiple nuclear factors interact with the immunoglobulin enhancer sequences
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175. IKKα is essential for protecting T cells from TNFα-induced apoptosis
176. Targeted disruption of the p50 subunit of NF-κB leads to multifocal defects in immune responses
177. Toxoplasma gondii actively inhibits activation of NF-κB
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179. Interaction of NF-κB and NFAT with the interferon-promoter
180. Genomic rearrangement in NEMO impairs NF-κB activation and is a cause of incontinentia pigmenti
181. B cells lacking RelB are defective in proliferative responses, but undergo normal B cell maturation to Ig secretion and Ig class switching
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226. The prosurvival Bcl-2 homolog Bfl-1/A1 is a direct transcriptional target of NF-κB that blocks TNFα-induced apoptosis