Modulation of plasmacytoid dendritic cell and CD4+ T cell differentiation accompanied by upregulation of the cholinergic anti-inflammatory pathway induced by enterovirus 71
Li LiRongwei HuangXiaoning LiuXiao-Yi XiangYuantao ZhouXing-Xing FengLv-Yuan TaoJia YuQin YiYanchun WangXiao-Mei Liu
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Abstract Vitamin A and its biologically active metabolites, all-trans and 9-cis retinoic acid (RA), are thought to be important in generating and modulating immune function. However, RA modulates the function of many types of immune cells, and its specific role in dendritic cell (DC) activation, Ag presentation, and T cell effector function has not been fully characterized. Because RA works primarily through RA receptor (RAR)α, we examined mice with a myeloid cell–specific defect in RA signaling. These transgenic mice have a CD11c-cre–driven expression of a truncated form of RARα that specifically blocks the signaling of all forms of RARs in myeloid cells. This defect results in abnormal DC function, with impaired DC maturation and activation, and reduced Ag uptake and processing. These DC abnormalities were associated with a reduced ability to mount Ag-specific T cell responses to immunization despite having normally functioning T cells. In contrast, the loss of DC-specific RA signaling did not significantly alter levels of Ag-specific Abs postimmunization and resulted in an increase in bronchial IgA. Our findings indicate that RA signaling in DCs is crucial for immune activation, and its absence impairs the development of Ag-specific effector functions of T cell immunity.
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Proinflammatory cytokines traditionally thought to be derived exclusively from the immune system and were therefore considered to be primarily responsible for initiating inflammatory in the myocardium. The effects of Proinflammatory Cytokines in the heart were discussed.
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Proinflammatory cytokines such as tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1) have been found to be elevated in bronchoalveolar lavage (BAL) fluid and in plasma from patients with acute respiratory distress syndrome (ARDS). In order to measure the balance of proinflammatory cytokines and their inhibitors, we quantified the upregulation of intercellular adhesion molecules (ICAM-1) induced by ARDS BAL fluids in human alveolar type II-like (A459) cells, and defined proinflammatory activity as the amount of ICAM-1 induced by the SAL fluids. Proinflammatory activity was detected in 77% of the SAL fluids sampled during the first week of ARDS, was found maximal during the 3 first days after onset of ARDS, and was significantly greater than in BAL specimens from at risk patients. Blocking experiments with specific inhibitors of TNF and IL-1 added to the BAL fluids indicated that the bioactivity measured was mainly due to IL-1. In contrast, proinflammatory activity of conditioned supernates from endotoxin-treated alveolar macrophages was mostly due to TNF. Using a bioassay that measures balance of cytokines with their inhibitors, our results indicate that the net proinflammatory activity in ARDS BAL fluids is attributable to IL-1 and not to TNF.
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Abstract Objectives The study was to explore the influence of microRNA (miR)-345-3p on proinflammatory cytokines in patients with rheumatoid arthritis (RA). Methods A total of 32 RA patients and 32 healthy patients were enrolled. Proinflammatory factors in patients’ serum were detected by ELISA, and miR-345-3p was detected by RT-qPCR. The correlation between miR-345-3p expression and proinflammatory factors in RA patients was analyzed. The diagnostic value of miR-345-3p and proinflammatory factors in RA patients was analyzed by receiver operating curve diagnosis. The predictive value of miR-345-3p levels and proinflammatory factors in RA patients was analyzed by multivariate Cox regression. HFLS-RA and HFLS cells were cultured, in which miR-345-3p and proinflammatory cytokines were detected by RT-qPCR. Cell proliferation and apoptosis were determined by CCK-8 and flow cytometry, respectively. Results MiR-345-3p was lowly expressed in the serum of RA patients. MiR-345-3p and proinflammatory factors were of diagnostic and predictive values in RA. Elevated miR-345-3p restrained the production of proinflammatory factors of HFLS-RA cells, improved cell proliferation, and reduced apoptosis. Conclusion MiR-345-3p is a potential biomarker and ameliorates RA by reducing the release of proinflammatory cytokines.
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The brain's response to ischemic injury is an acute and long-term inflammatory process. This process involves activation of resident cells (mainly microglia, hematogenous macrophages), production of proinflammatory mediators and infiltration of various proinflammatory cells (mainly neutrophils and lymphocytes). These cells play an essential role in ischemic brain tissue by releasing either proinflammatory or anti-inflammatory mediators at different time points. However, the exact pathogenesis of proinflammatory or anti-inflammatory genes in this process has not yet been elucidated. This review aims to investigate the inflammatory process of stroke, especially the role of proinflammatory and anti-inflammatory genes in the pathogenesis of stroke. We also summarize the current clinical trials of drugs that target the inflammatory mechanism for intervention.
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Abstract Mutations of the common cytokine receptor gamma chain (gc) cause Severe Combined Immunodeficiency characterized by absent T and NK cell development. Although these lineages are restored by stem cell therapy, residual immune defects are observed that may result from a selective persistence of gc-deficiency in myeloid lineages. However, little is known about the contribution of myeloid-expressed gc to protective immune responses. We examined the importance of gc for myeloid lineage dendritic cell (DC) function, and show that DC-expressed gc is required for effective antigen-induced CD4+ T cell activation. Using a novel lipid bilayer system mimicking T cell interaction, we observed that gc in DC was recruited to the contact interface following MHCII ligation, and promoted IL-15Ra colocalization with engaged MHCII. Unexpectedly, trans-presentation of IL-15 was required for optimal CD4+T cell activation by DC and depended on expression of gc in DC. These findings reveal a novel mechanism for recruitment of DC IL-15/IL-15Ra complexes to the immune synapse, leading to CD4+ T cell costimulation through localized IL-15 transpresentation that is coordinated with antigen-recognition.
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"Downregulation of miR-140-3p Is a Cause of Upregulation of RhoA Protein in Bronchial Smooth Muscle of Murine Experimental Asthma." American Journal of Respiratory Cell and Molecular Biology, 64(1), pp. 138–140
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Proinflammatory reaction by the body occurs acutely in response to injury that is considered primarily beneficial. However, sustained proinflammatory cytokines observed with chronic pathologies such as metabolic syndrome, cancer, and arthritis are detrimental and in many cases is a major cardiovascular risk factor. Proinflammatory cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor α (TNFα) have long been implicated in cardiovascular risk and considered to be a major underlying cause for heart failure (HF). The failure of the anti-TNFα therapy for HF indicates our elusive understanding on the dichotomous role of proinflammatory cytokines on acutely beneficial effects versus long-term deleterious effects. Despite these well-described observations, less is known about the mechanistic underpinnings of proinflammatory cytokines especially TNFα in pathogenesis of HF. Increasing evidence suggests the existence of an active cross-talk between the TNFα receptor signaling and G-protein-coupled receptors such as β-adrenergic receptor (βAR). Given that βARs are the key regulators of cardiac function, the review will discuss the current state of understanding on the role of proinflammatory cytokine TNFα in regulating βAR function.
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