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TNF — TSLP

Text-mined interactions from Literome

Koyama et al., Biochem Biophys Res Commun 2007 (Arthritis, Rheumatoid...) : In addition, TNF-alpha up-regulated TSLP expression in RA- and OA-derived synovial fibroblasts, which was inhibited by IFN-gamma
Zhang et al., Am J Physiol Lung Cell Mol Physiol 2007 (MAP Kinase Signaling System...) : Taken together, our data provide the first evidence of IL-1beta- and TNF-alpha induced TSLP expression in HASMC via ( p38, p42/p44 ) MAPK signaling pathways
Nonaka et al., American journal of rhinology & allergy 2010 (Chronic Disease...) : Nasal polyp fibroblasts have the capacity to produce TSLP in response to stimulation by tumor necrosis factor (TNF) alpha
Wu et al., Hum Reprod 2010 : IL-4 and TNF-alpha or pregnancy associated hormones result in a significant increase in TSLP mRNA expression and protein release from EVT, and TSLP promotes primary EVT proliferation and invasion in vitro
Le et al., Int Arch Allergy Immunol 2011 : The flagellin induced release of TSLP was enhanced by the Th2/TNF cytokines or TGF-a
Redhu et al., Am J Physiol Lung Cell Mol Physiol 2011 : Essential role of NF-?B and AP-1 transcription factors in TNF-a induced TSLP expression in human airway smooth muscle cells ... In this study, we found that TNF-a upregulates the TSLP mRNA and induces high levels of TSLP protein release in primary human ASM cells ... Interestingly, TNF-a induced the TSLP promoter activity ( P < 0.05 ; n = 4 ) in HASM that was mediated by upstream NF-?B and activator protein-1 (AP-1) binding sites ... Mutation in NF-?B and AP-1 binding sites completely abrogated the effect of TNF-a mediated TSLP promoter activity and so did the expression of a dominant negative mutant construct of I?B kinase ... Furthermore, the peptide inhibitors of I?B kinase or NF-?B inhibited the TNF-a induced TSLP protein release ( P < 0.05 ; n = 3 ) in HASM ... Collectively, our data suggest a novel important biological role for NF-?B pathway in TNF-a induced TSLP expression in HASM and recommend this as a prime target for anti-inflammatory drugs