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• W61403476 abstract "Idiopathic pulmonary fibrosis (IPF) is a progressive and typically fatal lung disease. To gain insight into the pathogenesis of IPF, we reanalyzed our previously published gene expression data profiling IPF lungs. Cytokine receptor-like factor 1 (CRLF1) was among the most highly up-regulated genes in IPF lungs, compared with normal controls. The protein product (CLF-1) and its partner, cardiotrophin-like cytokine (CLC), function as members of the interleukin 6 (IL-6) family of cytokines. Because of earlier work implicating IL-6 family members in IPF pathogenesis, we tested whether CLF-1 expression contributes to inflammation in experimental pulmonary fibrosis. In IPF, we detected CLF-1 expression in both type II alveolar epithelial cells and macrophages. We found that the receptor for CLF-1/CLC signaling, ciliary neurotrophic factor receptor (CNTFR), was expressed only in type II alveolar epithelial cells. Administration of CLF-1/CLC to both uninjured and bleomycin-injured mice led to the pulmonary accumulation of CD4(+) T cells. We also found that CLF-1/CLC administration increased inflammation but decreased pulmonary fibrosis. CLF-1/CLC leads to significantly enriched expression of T-cell-derived chemokines and cytokines, including the antifibrotic cytokine interferon-γ. We propose that, in IPF, CLF-1 is a selective stimulus of type II alveolar epithelial cells and may potentially drive an antifibrotic response by augmenting both T-helper-1-driven and T-regulatory-cell-driven inflammatory responses in the lung." @default.
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• W61403476 date "2012-05-01" @default.
• W61403476 modified "2023-09-28" @default.
• W61403476 title "Cytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs" @default.
• W61403476 cites W1530725542 @default.
• W61403476 cites W1533188705 @default.
• W61403476 cites W1548223836 @default.
• W61403476 cites W1557678369 @default.
• W61403476 cites W1585555176 @default.
• W61403476 cites W1778719309 @default.
• W61403476 cites W1836438695 @default.
• W61403476 cites W1967108732 @default.
• W61403476 cites W1970810728 @default.
• W61403476 cites W1972343772 @default.
• W61403476 cites W1973537311 @default.
• W61403476 cites W1975224746 @default.
• W61403476 cites W1979141644 @default.
• W61403476 cites W1981901332 @default.
• W61403476 cites W1985144240 @default.
• W61403476 cites W1988007182 @default.
• W61403476 cites W1990584310 @default.
• W61403476 cites W1994090580 @default.
• W61403476 cites W2009001235 @default.
• W61403476 cites W2009533207 @default.
• W61403476 cites W2017884496 @default.
• W61403476 cites W2018809578 @default.
• W61403476 cites W2023970331 @default.
• W61403476 cites W2026995229 @default.
• W61403476 cites W2027170202 @default.
• W61403476 cites W2028735077 @default.
• W61403476 cites W2031488553 @default.
• W61403476 cites W2035774221 @default.
• W61403476 cites W2038838786 @default.
• W61403476 cites W2039079142 @default.
• W61403476 cites W2045115383 @default.
• W61403476 cites W2049903387 @default.
• W61403476 cites W2051634042 @default.
• W61403476 cites W2059978214 @default.
• W61403476 cites W2070537009 @default.
• W61403476 cites W2073763489 @default.
• W61403476 cites W2074978939 @default.
• W61403476 cites W2075876102 @default.
• W61403476 cites W2081082633 @default.
• W61403476 cites W2081517449 @default.
• W61403476 cites W2082515801 @default.
• W61403476 cites W2084509745 @default.
• W61403476 cites W2087598571 @default.
• W61403476 cites W2091929727 @default.
• W61403476 cites W2095715691 @default.
• W61403476 cites W2097623374 @default.
• W61403476 cites W2098765934 @default.
• W61403476 cites W2099677690 @default.
• W61403476 cites W2105198579 @default.
• W61403476 cites W2108683967 @default.
• W61403476 cites W2111139868 @default.
• W61403476 cites W21131537 @default.
• W61403476 cites W2116654149 @default.
• W61403476 cites W2117564935 @default.
• W61403476 cites W2120446140 @default.
• W61403476 cites W2131029325 @default.
• W61403476 cites W2132084960 @default.
• W61403476 cites W2134215992 @default.
• W61403476 cites W2136114918 @default.
• W61403476 cites W2137064182 @default.
• W61403476 cites W2137157684 @default.
• W61403476 cites W2144212283 @default.
• W61403476 cites W2148482472 @default.
• W61403476 cites W2148507750 @default.
• W61403476 cites W2149410494 @default.
• W61403476 cites W2150066073 @default.
• W61403476 cites W2152555245 @default.
• W61403476 cites W2154490230 @default.
• W61403476 cites W2158217645 @default.
• W61403476 cites W2162149101 @default.
• W61403476 cites W2162977751 @default.
• W61403476 cites W2163989802 @default.
• W61403476 cites W2164998164 @default.
• W61403476 cites W2167646969 @default.
• W61403476 cites W2169624176 @default.
• W61403476 cites W2170870273 @default.
• W61403476 cites W2315096416 @default.
• W61403476 cites W4249234705 @default.
• W61403476 doi "https://doi.org/10.1016/j.ajpath.2012.01.010" @default.
• W61403476 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3354590" @default.

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