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Uteroglobin suppresses allergen‐induced T H 2 differentiation by down‐regulating the expression of serum amyloid A and SOCS‐3 genes
Author(s) -
Ray Rabindranath,
Zhang Zhongjian,
Lee Yi-Ching,
Gao Ji-Liang,
Mukherjee Anil B.
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.09.059
Subject(s) - uteroglobin , immunology , allergic inflammation , inflammation , chemotaxis , population , secretion , biology , chemistry , microbiology and biotechnology , receptor , gene , medicine , endocrinology , genetics , environmental health
Allergen‐induced airway inflammation may lead to allergic asthma, a chronic inflammatory disease of the respiratory system. Despite its high incidence, the majority of the world's population is unaffected by allergic airway inflammation most likely due to innate protective mechanism(s) in the respiratory system. The mammalian airway epithelia constitutively express uteroglobin (UG), a protein with potent anti‐inflammatory and anti‐chemotactic properties. We report here that UG binds to FPR2, a G‐protein coupled receptor, inhibits chemotaxis, down‐regulates SOCS‐3 gene expression and STAT‐1 activation, which are critical for the differentiation of T‐helper 2 (T H 2) cells that secrete pro‐inflammatory T H 2 cytokines. We propose that UG suppresses allergen‐mediated activation of T H 2 response by down‐regulating the expression of genes that are critical for T H 2 differentiation.