Uteroglobin suppresses allergen-induced TH2 differentiation by down-regulating the expression of serum amyloid A and SOCS-3 genes |
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Authors: | Ray Rabindranath Zhang Zhongjian Lee Yi-Ching Gao Ji-Liang Mukherjee Anil B |
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Affiliation: | Section on Developmental Genetics, Heritable Disorders Branch, National Institute of Child Health and Human Development, The National Institutes of Health, Building 10, Rm 9D42, 10, Center Drive, Bethesda, MD 20892-1830, USA. |
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Abstract: | 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. |
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Keywords: | UG, uteroglobin UG-KO, uteroglobin-knockout CC10, Clara cell 10 kDa protein OVA, ovalbumin SAA, serum amyloid A FPR, formyl peptide receptor TH2 cells, T-helper 2 cells DCs, dendritic cells SOCS-3, suppressor of cytokine signaling-3 |
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