Recruitment of CCR6-Expressing Th17 Cells by CCL 20 Secreted from IL-1β-, TNF-α-, and IL-17A-Stimulated Endometriotic Stromal Cells

Hirata, Tetsuya; Osuga, Yutaka; Takamura, Masashi; Kodama, Ako; Hirota, Yasushi; Koga, Kaori; Yokosuka, Osamu; Harada, Miyuki; Takemura, Yuri; Yano, Tetsu; Taketani, Yuji

doi:10.1210/en.2010-0398

Cited by 97 publications

(82 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…After investigation, our study showed that cardiac fibroblasts rather than cardiomyocytes were the main cardiogenic CCL20-releasing cells stimulated in vitro . Previously, Hirata et al reported that TNF-α, IL-1β and IL-17 coud activate the CCL20 promoter AP-1 and mediate the CCL20 expression at the transcriptional level [24,25,26]. In this study, the CCL20 expressions in cardiac fibroblasts were also be regulated by those specific cytokines, which might be indicated that there was no molecular difference in CCL20 from cardiac fibroblasts and other proinflammatory cells.…”

Section: Discussionsupporting

confidence: 48%

Cardiac Fibroblasts Recruit Th17 Cells Infiltration Into Myocardium by Secreting CCL20 in CVB3-Induced acute Viral Myocarditis

Zhu

et al. 2013

Cell Physiol Biochem

View full text Add to dashboard Cite

Aims: Th17 cells contributed to myocardial inflammatory injury in acute viral myocarditis (AVMC), and the migration of these cells were mainly mediated by CCL20-secreting inflammatory cells. However, whether and how the resident cells such as cardiomyocytes and cardiac fibroblasts could mediate Th17 cell migration into the heart remains unclear in AVMC. Methods: The effect of CCL20 on the dynamic alterations of intracardiac Th17 cells and disease severity were investigated through the neutralization of CCL20 in AVMC mice. The key cells releasing CCL20 in the heart and the effects of CCL20-secreting cells on Th17 cell arrest, migration and differentiation were detected in vitro. Results: Neutralization of CCL20 efficiently repressed the myocardial inflammation along with the reduction of Th17 cell infiltrations in the course of AVMC. In vitro, after stimulations of TNF-α, IL-1β and IL-17, cardiac fibroblasts rather than cardiomyocytes could be dominantly induced for CCL20 production. CCL20-secreting cardiac fibroblasts boosted Th17 cell arrest on endothelium, and induce Th17 cell migration. However, CCL20 produced by cardiac fibroblasts had no effect on Th17 cell differentiation and IL-17 production. Conclusions: It firstly suggested that cardiac fibroblasts could recruit Th17 cells infiltration into myocardium by secreting CCL20 in AVMC.

show abstract

Section: Discussionsupporting

confidence: 48%

Cardiac Fibroblasts Recruit Th17 Cells Infiltration Into Myocardium by Secreting CCL20 in CVB3-Induced acute Viral Myocarditis

Zhu

et al. 2013

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…6E). We also detected the expressions of CXCL-9, CXCL-10, CXCR-3, and CCL-20, which have been reported to be associated with Th1 and Th17 cell recruitments (9,12,30,33). Gal-9 downregulated the intrarenal mRNA expressions of CXCL-9, CXCR-3, and CCL-20 at days 21 and 28 (Fig.…”

Section: Cd4 ϩ Tim-3 ϩ T Cells Are Increased In Anti-gbm Gnmentioning

confidence: 71%

Galectin-9 ameliorates anti-GBM glomerulonephritis by inhibiting Th1 and Th17 immune responses in mice

Zhang

Luan

Wang

et al. 2014

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

Antiglomerular basement membrane glomerulonephritis (anti-GBM GN) is a Th1- and Th17-predominant autoimmune disease. Galectin-9 (Gal-9), identified as the ligand of Tim-3, functions in diverse biological processes and leads to the apoptosis of CD4(+)Tim-3(+) T cells. It is still unclear how Gal-9 regulates the functions of Th1 and Th17 cells and prevents renal injury in anti-GBM GN. In this study, Gal-9 was administered to anti-GBM GN mice for 7 days. We found that Gal-9 retarded the increase of Scr, ameliorated renal tubular injury, and reduced the formation of crescents. The infiltration of Th1 and Th17 cells into the spleen and kidneys significantly decreased in Gal-9-treated nephritic mice. The reduced infiltration of Th1 and Th17 cells might be associated with the downregulation of CCL-20, CXCL-9, and CXCL-10 mRNAs in the kidney. In parallel, the blood levels of IFN-γ and IL-17A declined in Gal-9-treated nephritic mice at days 21 and 28. In addition, an enhanced Th2 cell-mediated immune response was observed in the kidneys of nephritic mice after a 7-day injection of Gal-9. In conclusion, the protective role of Gal-9 in anti-GBM GN is associated with the inhibition of Th1 and Th17 cell-mediated immune responses and enhanced Th2 immunity in the kidney.

show abstract

“…The inhibitory effect of these inhibitors is also observed in IL-1b-induced secretion of IL-8 and CCL20 from ESCs (Yoshino et al, 2004;Hirata et al, 2010), both of which are suggested to stimulate inflammation in endometriosis. Accordingly, these MAPK inhibitors may hinder the progression of the disease by suppressing both inflammation and Th2 immune response.…”

Section: Discussionmentioning

confidence: 91%

Interleukin-1β stimulates the secretion of thymic stromal lymphopoietin (TSLP) from endometrioma stromal cells: possible involvement of TSLP in endometriosis

et al. 2012

Self Cite

View full text Add to dashboard Cite

study question: Is thymic stromal lymphopoietin (TSLP) involved in the pathophysiology of endometriosis? summary answer: TSLP is up-regulated by interleukin (IL)-1b and may be involved in the development of endometriosis. what is known already: Endometriosis is a chronic inflammatory disease in which the Th2 immune response is activated and has been suggested to promote the disease. TSLP is a master cytokine that drive Th2 immune response. study design, size, duration: A laboratory study. participants/materials, setting, methods: Primary cultures of endometrioma stromal cells (ESCs) were treated with IL-1b, a typical inflammatory cytokine associated with endometriosis. Gene expression of TSLP in ESCs and secretion of TSLP protein from ESCs were studied using quantitative PCR and a specific ELISA. Interferon g (IFNg), a typical Th1 cytokine, and IL-4, a typical Th2 cytokine, were added to the culture to evaluate their effect on the IL-1b-induced secretion of TSLP. Inhibitors of p38 mitogen-activated protein kinase (MAPK), p42/44 MAPK and stress-activated protein kinase/Jun amino-terminal kinase (SAPK/JNK) were added to the culture to examine intracellular signals involved in IL-1b-induced TSLP secretion. The expression of TSLP in endometrioma tissue was examined by immunohistochemistry. The concentration of TSLP in the serum and peritoneal fluid (PF) of women with or without endometriosis was measured with a specific ELISA.main results and the role of chance: IL-1b stimulated the expression of TSLP mRNA and secretion of TSLP protein from ESCs. IL-4 enhanced the IL-1b-induced TSLP secretion from ESCs, while IFNg reduced it. Inhibitors of p42/44 MAPK, p38 MAPK and SAPK/JNK suppressed the IL-1b-induced secretion of TSLP from ESCs. Positive immunostaining of TSLP was observed in the stroma of endometrioma tissue. TSLP concentrations in the serum and PF were both higher in women with endometriosis compared with those without endometriosis.limitations, reasons for caution: The present study was only in vitro. The samples used for culture were endometrioma tissues, not including other types of endometriosis. Therefore, the present findings should be interpreted with caution.wider implications of the findings: This study provided new insights in the Th2 immune response-related mechanism in endometriosis.

show abstract

Recruitment of CCR6-Expressing Th17 Cells by CCL 20 Secreted from IL-1β-, TNF-α-, and IL-17A-Stimulated Endometriotic Stromal Cells

Cited by 97 publications

References 30 publications

Cardiac Fibroblasts Recruit Th17 Cells Infiltration Into Myocardium by Secreting CCL20 in CVB3-Induced acute Viral Myocarditis

Cardiac Fibroblasts Recruit Th17 Cells Infiltration Into Myocardium by Secreting CCL20 in CVB3-Induced acute Viral Myocarditis

Galectin-9 ameliorates anti-GBM glomerulonephritis by inhibiting Th1 and Th17 immune responses in mice

Interleukin-1β stimulates the secretion of thymic stromal lymphopoietin (TSLP) from endometrioma stromal cells: possible involvement of TSLP in endometriosis

Contact Info

Product

Resources

About