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CXCL5 — IL17A
Text-mined interactions from Literome
Rahman et al., Clin Immunol 2005
:
IL-17R activation of human airway smooth muscle cells
induces CXCL-8 production via a transcriptional dependent mechanism ... While it has been shown that IL-17 induces expression of the CXC chemokines in the airways leading to neutrophil recruitment, the IL-17R expression in human ASM cells and the molecular mechanism by which
IL-17 mediates neutrophilic chemo-attractant
CXCL-8 ( IL-8 ) production have not been determined ... Furthermore, IL-17 induction of CXCL-8 mRNA and protein release from ASM cells was abrogated by transcriptional inhibitor actinomycin D. CXCL-8 promoter reporter analysis using wild type and site specific mutant constructs demonstrated a key role for AP1 and NF-kappaB binding sites in
IL-17 induced
CXCL-8 expression ... These data demonstrate that
IL-17 mediates
CXCL-8 expression in ASM cells via a transcriptional mechanism depending on NF-kappaB and AP-1 pathways
Dragon et al., Am J Physiol Lung Cell Mol Physiol 2007
:
IL-17 enhances IL-1beta mediated
CXCL-8 release from human airway smooth muscle cells ... In this study, we evaluated whether
IL-17 could
enhance IL-1beta mediated
CXCL-8 release from human airway smooth muscle cells ( HASMC ) and investigated the upstream and downstream signaling events regulating the induction of CXCL-8
Lee et al., J Immunol 2008
:
IL-17 strongly repressed TNF-alpha stimulated expression of CXCL10, CXCL11, and CCL5, but
synergized with TNF-alpha for induction of
CXCL8 , CXCL1, and CCL20 mRNAs ... In contrast,
IL-17 represses expression of CXCL10,
CXCL11 , and CCR5, three chemokines that selectively recruit Th1 but not other effector T cells
Liu et al., J Immunol 2011
(Acute Lung Injury...) :
Because the T cell derived cytokine IL-17A enhances host defense by triggering production of chemokines, particularly in combination with TNF-a, we hypothesized that
IL-17A would
enhance TNF-a induced expression of
CXCL5 ... Using differentiated alveolar epithelial type II ( ATII ) cells derived from human fetal lung, we found that
IL-17A enhanced TNF-a induced CXCL5 transcription and
stabilized TNF-a induced
CXCL5 transcripts
Chen et al., PloS one 2011
:
IL-17A significantly
enhanced the production of
CXCL8 , CCL2, CCL20 and IL-6 by these cells
Takahashi et al., Eur J Oral Sci 2011
:
We evaluated the
effects of
IL-17 on the expression of
CXCL8 and CCL2 by HGECs using quantitative real-time PCR and ELISA ... Stimulation with
IL-17 up-regulated the secretion of
CXCL8 protein, but not the secretion of CCL2 protein ... The
effect of
IL-17 on
CXCL8 production was suppressed using an anti-IL-17R Ig, suggesting a role for a specific receptor-ligand interaction ... In conclusion,
IL-17 is
involved in the regulation of the innate immune response in HGECs by inducing
CXCL8 production
Novitskiy et al., Cancer Discov 2011
(Breast Neoplasms...) :
We report that
IL-17 significantly
increases the secretion of CXCL1 and
CXCL5 from mammary carcinoma cells, which is downregulated by TGF-ß through the type II TGF-ß receptor ( TßRII )
Li et al., Cell Immunol 2013
(Graves Disease) :
These changes facilitate the
IL-17 mediated upregulation of IL-6,
CXCL10 , and ICAM-1
Al-Alwan et al., J Immunol 2013
(Airway Remodeling...) :
Previously, we established that
IL-17 induced ( CXCL1,
CXCL2 , and CXCL3 ) production promoted airway smooth muscle cell ( ASMC ) migration, and consequently we sought to investigate the molecular mechanism of CXC induced ASMC migration