Cooperative Activation of CCL5 Expression by TLR3 and Tumor Necrosis Factor-α or Interferon-γ through Nuclear Factor-ĸB or STAT-1 in Airway Epithelial Cells
Author(s) -
Tetsuya Homma,
Satoshi Matsukura,
Takashi Hirose,
Tsukasa Ohnishi,
Teruaki Kimura,
Masatsugu Kurokawa,
Koushi Ieki,
Miho Odaka,
Shintaro Suzuki,
Shin Watanabe,
Masayuki Sato,
Mio Kawaguchi,
Robert P. Schleimer,
Mitsuru Adachi
Publication year - 2010
Publication title -
international archives of allergy and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.696
H-Index - 100
eISSN - 1423-0097
pISSN - 1018-2438
DOI - 10.1159/000312120
Subject(s) - ccl5 , microbiology and biotechnology , biology , tlr3 , tumor necrosis factor alpha , immunology , toll like receptor , immune system , t cell , il 2 receptor , innate immune system
CCL5/RANTES contributes to prolonged eosinophilic inflammation and asthma exacerbation after a viral infection. We studied the mechanism of CCL5 expression using viral product double-stranded RNA (dsRNA), a ligand of Toll-like receptor 3 (TLR3), and inflammatory cytokines in airway epithelial cells.
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