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CCL20 — IRF6

Text-mined interactions from Literome

Schutyser et al., J Immunol 2000 (Cell Transformation, Neoplastic) : Although coinduced with monocyte chemotactic protein-1 (MCP-1) and IL-8 by dsRNA, measles virus, and IL-1beta in diploid fibroblasts, leukocytes produced LARC/MIP-3alpha only in response to LPS
Sugita et al., J Immunol 2002 : Furthermore, pretreatment with gliotoxin, an inhibitor of NF-kappaB activity, abrogated the P. acnes/LPS induced MIP-3alpha expression of wild-type mice
Scapini et al., Eur J Immunol 2002 : Finally, we demonstrate that activation of p38 mitogen activated protein kinase ( MAPK ) plays an important role in mediating the production of CCL20 induced by LPS ( with or without IFN-gamma ), whereas activation of p42/44 extracellular signal regulated kinases ( ERK ) is involved in the enhancing effect of fMLP
Crane-Godreau et al., Infect Immun 2005 : Time course studies of CCL20 and TNF-alpha release in response to Pam ( 3 ) Cys and LPS indicated that CCL20 release peaked between 2 and 4 h after treatment, whereas TNF-alpha release was gradual over the length of the incubation
Hosokawa et al., Clin Exp Immunol 2005 : On the other hand, we found that not only NF-kappaB, p38 MAPK and ERK but also c-Jun NH2-terminal kinase (JNK) are involved in CCL20 production induced by E. coli LPS ... Taken together, these findings that HGF will be a source of CCL20 in periodontal tissue, and the CCL20 production will be controlled by proinflammatory cytokine and bacterial LPS in periodontally diseased tissue
Soboll et al., Immunology 2006 : Moreover, when added to the culture media along with LPS, oestradiol inhibited LPS induced increases in CCL20/MIP-3 alpha secretion into both the apical and basolateral compartments
Veerayutthwilai et al., Oral Microbiol Immunol 2007 (Dental Caries) : LPS up-regulated IL-1beta, tumor necrosis factor-alpha (TNF-alpha), CCL20 , hBD2, IL-8, TLR2 and TLR4 ; however, Pam3CSK4 down-regulated these mRNAs
Marcet et al., J Cell Physiol 2007 : Furthermore, UTP had no effect on interleukin-(IL)-8 release and reduced the release of both CCL20 and IL-8 induced by TNF-alpha and LPS
Ovrevik et al., Toxicology 2009 (Lung Neoplasms) : After 10h exposure, silica induced significantly increased expression of CCL20, CXCL1/-3/-8/-10/-11, lymphotoxin (LT)beta and interleukin (IL)-6 ; ufCB induced CXCL8/-10 and -11 ; ZnCl ( 2 ) induced CCL11/-20/-26, CXCL1/-5/-8/-14 and tumor necrosis factor (TNF)-alpha ; FeSO ( 4 ) induced a weak up-regulation of CXCL8 and TNF-alpha ; LPS induced CCL20 , CXCL1/-5/-8/-10/-11, LTbeta and IL-6 ; and 1-NP induced expression of CCL20, CXCL1/-3/-8, TNF-alpha and IL-6
Sheldon et al., PloS one 2010 : Stromal and epithelial cells isolated from the endometrium of WT but not Tlr4 ( -/- ) mice, secreted IL-6, CXCL1, CCL20 and prostaglandin E ( 2 ) in response to LPS , in a concentration and time dependent manner
Yamamoto et al., J Immunol 2012 (Pneumonia, Pneumococcal) : In response to LPS , only 2 of 84 cytokine transcripts ( CCL20 and CXCL5 ) were blunted in lungs of mutants, suggesting that a very limited subset of immune mediators is selectively elaborated by the alveolar epithelium