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Contribution of regulatory T cells to immune tolerance and association of microRNA‑210 and Foxp3 in preeclampsia.

Increasing evidence suggests that an exaggerated maternal systemic inflammatofrery response may play a central role in the pathogenesis of preeclampsia (PE). Considering the growing evidence on microRNAs (miRNAs) and tissue‑specific regulators of gene expression, we investigated the potential association of miR‑210 and forkhead box p3 (Foxp3) in preeclamptic patients. Serum levels of the cytokines interleukin (IL)‑6, IL‑10, IL‑17, and transforming grown factor‑β1 were detected with ELISA. Reverse‑transcription‑quantitative polymerase chain reaction was performed to detect mRNA expression for maternal placenta retinoic acid‑related orphan receptor C, Foxp3 and miRNA (miR)‑210. Foxp3 protein expression was evaluated by western blot analysis. Serum levels of cytokines IL‑10 were significantly lower in preeclamptic patients than in normal pregnant women. mRNA expression of Foxp3 was significantly lower in placenta of PE. mRNA expression of miR‑210 was significantly increased in PE. Results of western blot analysis indicated that Foxp3 protein expression was lower in PE than in normal pregnant women. Our data suggest that PE manifests as a decreased number of regulatory T cells (Tregs), which regulate maternal tolerance of the fetus. In placenta from women with PE, compared with normal pregnant women, mRNA expression of Foxp3 was significantly decreased, and expression of miR‑210 was significantly increased.

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MicroRNA 26a Expression in Peripheral Blood Mononuclear Cells and Correlation with Serum Interleukin-17 in Relapsing-Remitting Multiple Sclerosis Patients.

Multiple sclerosis (MS) is a chronic multifocal inflammatory demyelinating disease. One of the main cells that play a crucial role in pathogenesis of MS is T helper 17 (Th 17). There are growing interests in nominating microRNAs in Th17 cell differentiation and suggesting new therapeutic modalities. The aim of the study was to assess microRNA 26a (miR26a) expression in peripheral blood mononuclear cells of relapsing - remitting MS patients as compared to healthy control subjects and examine association of these levels with serum IL17. Forty (40) relapsing - remitting MS patients were enrolled based on the MacDonald criteria (20 in relapsing phase and 20 in remitting phase). In addition, twenty (20) healthy control subjects were included. Blood samples were subjected to quantitative polymerase chain reaction (qPCR) for miR26a and ELISA for serum IL 17 levels. A significant upregulation of miR26a relative expression level (∆∆ Ct) and serum IL17 level (pg/ml) was found in total MS patients and remitting MS patients when compared with controls (P < 0.001). Among the relapsing group, a significant increase in miR26a expression levels (P= 0.004) but not serum IL17 level was demonstrated. Insignificant correlation between miR26a expression and serum IL17 in MS patients was detected (r= 0.08, P= 0.62). In conclusion, a significant increase of these two biomarkers (miR26a & IL17) occurs in relapsing - remitting MS patients, and this reflects their important role in pathogenesis and disease development.

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IL‑17 induces NSCLC A549 cell proliferation via the upregulation of HMGA1, resulting in an increased cyclin D1 expression.

Non-small cell lung cancer (NSCLC) is considered to be an inflammation-associated carcinoma. Although interleukin‑17 (IL‑17) production contributes to the proliferation and growth of NSCLC, the mechanisms underlying IL‑17-induced NSCLC cell proliferation have not been fully elucidated. In the present study, by using ELISA and immunohistochemical analyses, we first found that the expression levels of IL‑17, IL‑17 receptor (IL‑17R), high-mobility group A1 (HMGA1) and cyclin D1 were elevated in the samples of patients with NSCLC. Subsequently, by RT-qPCR, western blot analysis and cell proliferation assay in vitro, we revealed that stimulation with recombinant human IL‑17 (namely IL‑17A) markedly induced the expression of HMGA1 and cyclin D1 in the A549 cells (a human lung adenocarcinoma cell line) and promoted cell proliferation. Furthermore, luciferase reporter and ChIP assays confirmed that upregulated HMGA1 directly bound to the cyclin D1 gene promoter and activated its transcription. Notably, the response element of HMGA1 binding to the cyclin D1 promoter was disclosed for the first time, at least to the best of our knowledge. Taken together, our findings indicate that the IL‑17/HMGA1/cyclin D1 axis plays an important role in NSCLC cell proliferation and may provide new insight into NSCLC pathogenesis and may thus aid in the development of novel therapeutic targets for NSCLC.

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Interleukin-17 induces angiogenesis in vitro via CXCL8 and CCL2 in retinal pigment epithelium.

Interleukin-17 (IL-17) is a major pro-inflammatory cytokine involved in choroidal endothelial cell (CEC) angiogenesis. Proteins expressed by the retinal pigment epithelium (RPE) may contribute to CEC angiogenesis. The ability of IL‑17 to promote proliferation, migration and capillary‑like structure formation in CECs was investigated by stimulating the RPE in vitro. CECs were cultured in a conditioned medium (CM) with IL‑17 (IL‑17‑CM) or without IL‑17 (CM) obtained from the supernatant of an ARPE‑19 cell line. The pro‑angiogenic role of IL‑17‑CM on CECs was investigated with water‑soluble tetrazolium 1 analysis, wound healing and Matrigel matrix tube formation assays. The expression level of vascular endothelial growth factor was detected by enzyme‑linked immunosorbent assay in RPE cells treated with or without IL‑17. Ras‑related C3botulinum toxin substrate 1 (Rac1) and Ras homolog gene family member A (RhoA) activities were analyzed by pull‑down assays. IL‑17‑CM significantly enhanced tube formation and increased the migration distance in CECs in comparison with CM. This effect was diminished by neutralizing C‑C motif chemokine 2 (CCL2) and C‑X‑C motif chemokine ligand 8 (CXCL8) expression in IL‑17‑CM, with a concomitant downregulation of Rac1 and RhoA activity in CECs. In conclusion, it was demonstrated that IL‑17 mediated the expression of CCL2 and CXCL8 in RPE cells, resulting in increased migration and tube formation in human CECs.

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Lower level of IL‑35 and its reduced inhibition in Th17 cells in patients with bone marrow mononuclear cells Coombs test‑positive hemocytopenia.

Interleukin (IL)-35 is the latest member of IL-12 family, which plays an important role in other autoimmune diseases. Bone marrow mononuclear cells Coombs test‑positive hemocytopenia, also termed immunorelated hemocytopenia (IRH) is a type of autoimmune-associated diseases. The present study investigated the relationship of IL‑35 in patients with IRH. A total of 43 patients with IRH and 19 normal controls were enrolled in the current study. Serum levels of IL‑35 and IL‑17 in peripheral blood were evaluated by ELISA. Regulatory T cells (Tregs) level was detected by flow cytometry and IL‑35 subunits mRNA in Treg was determined using reverse transcription‑quantitative polymerase chain reaction: Epstein‑Barr virus induced 3 (EBI3) and IL‑12α chain p35. Effect of IL‑35 on T helper 17 cells (Th17) cells was determined by mix‑culture of IL‑35 with CD4+ T lymphocytes. Serum level of IL‑35 was decreased in untreated patients with IRH compared with remission patients (P<0.01) and was significantly associated with clinical indexes. Frequency of IL‑35 produced Tregs was lower and IL‑35 subunits mRNA in CD4+CD25+ Tregs were decreased in patients with IRH compared with health controls (P<0.01). Serum level of IL‑17 was increased in patients with IRH (P<0.01) and there was a negative correlation between IL‑35 and IL‑17 (r=‑0.553; P<0.01). The production of Th17 cells and IL‑17A mRNA expression were reduced (P<0.05) after mix‑culture of CD4+ T lymphocytes with IL‑35 compared with mix‑culture of CD4+ T lymphocytes without IL‑35. In conclusion, the present study revealed that IL‑35 may be a monitoring indicator of IRH occurrence and progression. IL‑35 level was lower and the inhibition on Th17 cells was reduced in the patients with IRH.

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Increase in circulating Th17 cells during anti-TNF therapy is associated with ultrasonographic improvement of synovitis in rheumatoid arthritis.

Anti-TNF agents have revolutionised rheumatoid arthritis (RA) treatment; however, a third of patients fail to achieve therapeutic responses. Unexpectedly, studies in murine and human arthritis have indicated that anti-TNF treatment can increase circulating T helper 17 (Th17) cells, but the relationship to treatment response is unclear. To identify immune correlates of anti-TNF treatment response, we conducted a longitudinal study using clinical, ultrasound and T cell assessments.

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Diminished IL-17A levels may protect filarial-infected individuals from development of rheumatoid arthritis and systemic lupus erythematosus.

Nematode infections have been observed to inversely correlate with autoimmune disorders. Recently, we have shown the absence of filarial infection in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) who live in filarial-endemic areas. The mechanism(s) by which filarial-infected individuals are protected against the development of RA or SLE are unknown. In mice CIA, an experimental model for RA, ES-62, an execratory product of rodent filarial nematode , has been shown to improve arthritis through suppression of the IL-17 pathway. A total of 160 individuals, 40 each of endemic normal, filarial-infected cases, SLE and RA patients, from filarial-endemic areas, were enrolled in the study. Plasma levels of IL17-A, IFN-α and TNF-α were quantified by enzyme-linked immunosorbent assay (ELISA). RA and SLE patients displayed significantly higher plasma IL-17A, IFN-α and TNF-α levels compared to endemic normal and infected individuals. Furthermore, IL-17A levels were significantly low in participants with filarial infection compared to endemic controls ( p < 0.05). Interestingly, plasma IL-17A levels correlated inversely with circulating filarial antigen (CFA) ( p = 0.004, Spearman r = -0.51). Filarial infection was associated with low plasma IL-17A levels, a mechanism by which it possibly protects individuals in filarial-endemic areas from the development of autoimmune disorders like RA and SLE.

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Integrated analysis of the local and systemic changes preceding the development of post-partum cytological endometritis.

The regulation of endometrial inflammation has important consequences for the resumption of bovine fertility postpartum. All cows experience bacterial influx into the uterus after calving; however a significant proportion fail to clear infection leading to the development of cytological endometritis (CE) and compromised fertility. We hypothesised that early immunological changes could not only act as potential prognostic biomarkers for the subsequent development of disease but also shed light on the pathogenesis of endometritis in the postpartum dairy cow.

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Hypercholesterolemia Induced Immune Response and Inflammation on Progression of Atherosclerosis in Apob(tm2Sgy) Ldlr(tm1Her)/J Mice.

The effect of hypercholesterolemia induced immune response and inflammation on progression of atherosclerosis in ApoB(tm25gy) LDLr(tm1Her) mice, expressing only ApoB100 and deficient in the low density lipoprotein (LDL) receptor, thus closely resembling human cholesterol transport is not well defined. Atherosclerosis was induced by a high cholesterol diet and its progression was studied at 8, 14 and 20 weeks. Antibody response was determined by ELISA. Lymphocytes in spleen and aortic expression of inflammatory markers were studied by flow cytometry, and immunohistochemistry respectively. A rapid increase in plasma LDL levels in the first 8 weeks was followed by the exponential development of atherosclerosis between 8 and 14 weeks. Progression of the disease was accompanied by an accumulation of macrophages and increased expression of IL17 and IFN-γ in the aorta. Hypercholesterolemia resulted in increased immune response to modified lipids and aortic inflammation, with an expansion of Th17 cells in the spleen. Progression of atherosclerosis showed a positive correlation (r = 0.84, P < 0.001) with Th17 cells and a negative correlation with Treg cells (r = 0.83, P < 0.001). IgM antibodies to Ox-LDL and Th17 cells in spleen showed greatest association with disease development. Our results suggest that anti Ox-LDL IgM antibodies, Th17 cells could be developed as a potential marker to study disease progression and to study the effect of therapeutic regulation of inflammation.

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Multi-dose parecoxib provides an immunoprotective effect by balancing T helper 1 (Th1), Th2, Th17 and regulatory T cytokines following laparoscopy in patients with cervical cancer.

Analgesic treatment with anti‑inflammatory drugs may aid the prevention of postoperative pain and the attenuation of the postoperative immune inflammatory response. The current study presents a randomized, double‑blind controlled study, which was performed to investigate the levels of Th1, Th2, Th17 and Treg cytokines, including interleukin (IL)‑2, interferon (IFN)‑γ, IL‑4, IL‑10, IL‑17, IL‑23 and transforming growth factor (TGF)‑β in the peripheral blood of patients with cervical cancer following laparoscopy. The effects of perioperative multi‑dose parecoxib on postoperative immune function was evaluated. A total of 80 patients with cervical cancer (stage IB/IIA, ASA I‑III, aged 18‑65 years) that were scheduled for laparoscopy were randomly assigned into either the parecoxib (I; n=40) or control (II; n=40) groups. Group I received 40 mg parecoxib 30 min prior to surgery and then every 12 h subsequent to surgery for 60 h, and group II received normal saline at the corresponding time points. Intravenous tramadol (100 mg) was prescribed for pain relief as required. The mRNA and protein expression levels of cytokines in the peripheral blood were detected by quantitative polymerase chain reaction and ELISA. Pain visual analog scales (VAS) and incidence, analgesic relief, adverse events and the length of hospital stay were recorded. It was demonstrated that the mRNA and protein levels of IL‑2, IFN‑γ and IL‑17 in the two groups were reduced subsequent to surgery, while mRNA and protein expression levels of IL‑4, IL‑10 and TGF‑β were enhanced. Administration of multi‑dose parecoxib may diminish the increase in postoperative IL‑2, IFN‑γ and IL‑17 levels, and suppress the excessive production of IL‑4, IL‑10 and TGF‑β. This effect is accompanied by lower VAS scores, pain incidence, postoperative nausea/vomiting and infections. In conclusion, perioperative multi‑dose parecoxib was able to alleviate postoperative pain and ameliorate surgery‑induced immune suppression by balancing Th1, Th2, Th17 and Treg cytokines following laparoscopy in patients with cervical cancer. The current study provides support to the hypothesis that parecoxib may be a more effective therapeutic strategy than the currently available options, for postoperative pain and immune function management of patients with cancer.

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