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1.
Immun Inflamm Dis ; 12(3): e1209, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38456619

RESUMO

BACKGROUND: Immunosenescence is a multifactorial stress response to different intrinsic and extrinsic insults that cause immune deterioration and is accompanied by genomic or epigenomic perturbations. It is now widely recognized that genes and proteins contributing in the process of immunosenescence are regulated by various noncoding (nc) RNAs, including microRNAs (miRNAs), long ncRNAs, and circular RNAs. AIMS: This review article aimed to evaluate the regulatore RNAs roles in the process of immunosenescence. METHODS: We analyzed publications that were focusing on the different roles of regulatory RNAs on the several aspects of immunosenescence. RESULTS: In the immunosenescence setting, ncRNAs have been found to play regulatory roles at both transcriptional and post-transcriptional levels. These factors cooperate to regulate the initiation of gene expression programs and sustaining the senescence phenotype and proinflammatory responses. CONCLUSION: Immunosenescence is a complex process with pivotal alterations in immune function occurring with age. The extensive network that drive immunosenescence-related features are are mainly directed by a variety of regulatory RNAs such as miRNAs, lncRNAs, and circRNAs. Latest findings about regulation of senescence by ncRNAs in the innate and adaptive immune cells as well as their role in the immunosenescence pathways, provide a better understanding of regulatory RNAs function in the process of immunosenescence.


Assuntos
Imunossenescência , MicroRNAs , RNA Longo não Codificante , MicroRNAs/genética , RNA não Traduzido/genética , RNA não Traduzido/metabolismo , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , RNA Circular
2.
Front Immunol ; 14: 1077236, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-36793739

RESUMO

The current coronavirus pandemic (COVID-19), caused by SARS-CoV-2, has had devastating effects on the global health and economic system. The cellular and molecular mediators of both the innate and adaptive immune systems are critical in controlling SARS-CoV-2 infections. However, dysregulated inflammatory responses and imbalanced adaptive immunity may contribute to tissue destruction and pathogenesis of the disease. Important mechanisms in severe forms of COVID-19 include overproduction of inflammatory cytokines, impairment of type I IFN response, overactivation of neutrophils and macrophages, decreased frequencies of DC cells, NK cells and ILCs, complement activation, lymphopenia, Th1 and Treg hypoactivation, Th2 and Th17 hyperactivation, as well as decreased clonal diversity and dysregulated B lymphocyte function. Given the relationship between disease severity and an imbalanced immune system, scientists have been led to manipulate the immune system as a therapeutic approach. For example, anti-cytokine, cell, and IVIG therapies have received attention in the treatment of severe COVID-19. In this review, the role of immunity in the development and progression of COVID-19 is discussed, focusing on molecular and cellular aspects of the immune system in mild vs. severe forms of the disease. Moreover, some immune- based therapeutic approaches to COVID-19 are being investigated. Understanding key processes involved in the disease progression is critical in developing therapeutic agents and optimizing related strategies.


Assuntos
COVID-19 , Humanos , SARS-CoV-2 , Estado Terminal , Citocinas , Imunidade
3.
Immun Inflamm Dis ; 10(10): e715, 2022 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-36169248

RESUMO

INTRODUCTION: The frequencies and functions of T stem cell memory (TSCM) subsets vary in autoimmune diseases. We evaluated the frequencies of CD4+ and CD8+ TSCM subsets as well as their PD-1 expression levels in patients with T1D. METHODS: Blood samples were collected from new case (NC) (n = 15), and long-term (LT) (n = 15) groups and healthy controls (n = 15). Five subsets of T cells including TCM(CD4+ /CD8+ CCR7+ CD45RO+ CD95+ ), TCMhi (CD4+ /CD8+ CCR7+ CD45ROhi CD95+ ), TEM(CD4+ /CD8+ CCR7- CD45RO+ CD95+ ), TSCM(CD4+ /CD8+ CCR7+ CD45RO- CD95+ ), and T naive (CD4+ /CD8+ CCR7+ CD45RO- CD95- ) were detected by flow-cytometry. RESULTS: The frequency of CD4+ TSCM was higher in NC patients than LT patients and controls (p < .0001 and p = .0086, respectively). A higher percentage of the CD8+ T naive cells was shown in NC patients as compared with LT and healthy individuals (p = .0003 and p = .0002, respectively). An increased level of PD-1 expression was observed on the CD4+ TCM and TCMhi cells in LT patients as compared with healthy controls (p = .0037 and p = .0145, respectively). Also, the higher PD-1 expression was observed on the CD8+ TCM and TCMhi in NC and LT patients as compared with controls (p = .0068 and p < .0001; p = .0012 and p = .0012, respectively). CONCLUSION: Considering TSCMs' capacities to generate all memory and effector T cells, our results may suggest a potential association between the increased frequencies of TSCMs and T1D progression.


Assuntos
Diabetes Mellitus Tipo 1 , Memória Imunológica , Linfócitos T CD4-Positivos , Linfócitos T CD8-Positivos , Humanos , Receptor de Morte Celular Programada 1 , Receptores CCR7 , Células-Tronco
4.
Int Immunopharmacol ; 101(Pt A): 108295, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34735917

RESUMO

Toll-like receptors (TLRs) are among the players of inflammation during atherosclerosis. We assessed the effects of Eritoran, a TLR-4 antagonist, on lipopolysaccharide (LPS)-induced cytokines production by Peripheral Blood Mononuclear Cells (PBMCs) of patients with high-stenosis (HS) (n = 6) and healthy controls (HCs) (n = 6) co-cultured with Human Umbilical Vein Endothelial Cells (HUVECs). LPS stimulation significantly increased the levels of IL-6 (P = 0.007 and P = 0.005), TNF-α (P = 0.006 and P = 0.005), IL-2 (P = 0.007 and P = 0.002), IFN-γ (P = 0.006 and P = 0.003), IL-17A (P = 0.004 and P = 0.003), IL-17F (P = 0.005 and P = 0.003), IL-5 (P = 0.007 and P = 0.005), IL-13 (P = 0.006 and P = 0.005), IL-9 (P = 0.005 and P = 0.005) and IL-21 (P = 0.007 and P = 0.005) in HUVECs co-cultured with HC and HS PBMCs as compared with un-stimulated co-culture condition, respectively. Eritoran treatment (50 µg/mL and 100 µg/mL) significantly reduced the levels of LPS-induced IL-6 (P = 0.007 and P = 0.006; P = 0.007 and P = 0.007), TNF-α (P = 0.005 and P = 0.003; P = 0.007 and P = 0.005), IL-2 (P = 0.007 and P = 0.005; P = 0.005 and P = 0.004), IFN-γ (P = 0.007 and P = 0.005; P = 0.005 and P = 0.004), IL-17A (P = 0.005 and P = 0.002; P = 0.005 and P = 0.002), IL-17F (P = 0.006 and P = 0.006; P = 0.005 and P = 0.005), IL-5 (P = 0.007 and P = 0.006; P = 0.007 and P = 0.007), IL-9 (P = 0.005 and P = 0.005; P = 0.005 and P = 0.005) and IL-21 (P = 0.007 and P = 0.007; P = 0.005 and P = 0.005) in stimulated HUVECs co-cultured with HC and HS PBMCs, compared to un-treated condition, respectively. Our results demonstrate that attenuating effect of Eritoran on the inflammatory responses to LPS is higher in PBMCs of patients with high stenosis, suggesting its potential role in ameliorating inflammatory conditions in atherosclerosis.


Assuntos
Aterosclerose/imunologia , Citocinas/metabolismo , Dissacarídeos/farmacologia , Leucócitos Mononucleares/efeitos dos fármacos , Fosfatos Açúcares/farmacologia , Receptor 4 Toll-Like/antagonistas & inibidores , Adulto , Aterosclerose/tratamento farmacológico , Estudos de Casos e Controles , Técnicas de Cocultura , Dissacarídeos/uso terapêutico , Relação Dose-Resposta a Droga , Feminino , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/imunologia , Humanos , Interferon gama/metabolismo , Interleucina-17/metabolismo , Interleucina-2/metabolismo , Interleucina-6/metabolismo , Interleucina-9/metabolismo , Interleucinas/metabolismo , Leucócitos Mononucleares/metabolismo , Lipopolissacarídeos/farmacologia , Masculino , Pessoa de Meia-Idade , Fosfatos Açúcares/uso terapêutico , Fator de Necrose Tumoral alfa/metabolismo
5.
Artigo em Inglês | MEDLINE | ID: mdl-31622224

RESUMO

BACKGROUND AND OBJECTIVE: Atherosclerosis, a chronic and progressive inflammatory disease, is triggered by the activation of endothelial cells followed by infiltration of innate and adaptive immune cells including monocytes and T cells in arterial walls. Major populations of T cells found in human atherosclerotic lesions are antigen-specific activated CD4+ effectors and/or memory T cells from Th1, Th17, Th2 and Treg subsets. In this review, we will discuss the significance of T cell orchestrated immune inflammation in the development and progression of atherosclerosis. DISCUSSION: Pathogen/oxidative stress/lipid induced primary endothelial wound cannot develop to a full-blown atherosclerotic lesion in the absence of chronically induced inflammation. While the primary inflammatory response might be viewed as a lone innate response, the persistence of such a profound response over time must be (and is) associated with diverse local and systemic T cell responses. The interplay between T cells and innate cells contributes to a phenomenon called immuneinflammation and has an impact on the progression and outcome of the lesion. In recent years immuneinflammation, an old term, has had a comeback in connecting the puzzle pieces of chronic inflammatory diseases. CONCLUSION: Taking one-step back and looking from afar at the players of immune-inflammation may help us provide a broader perspective of these complicated interactions. This may lead to the identification of new drug targets and the development of new therapies as well as preventative measures.


Assuntos
Imunidade Adaptativa/fisiologia , Aterosclerose/imunologia , Aterosclerose/metabolismo , Imunidade Inata/fisiologia , Mediadores da Inflamação/imunologia , Mediadores da Inflamação/metabolismo , Animais , Humanos , Inflamação/imunologia , Inflamação/metabolismo , Linfócitos T/imunologia , Linfócitos T/metabolismo
6.
Int J Toxicol ; 36(2): 133-141, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28403739

RESUMO

Inflammation and oxidative stress are important risk factors affecting various cells in the formation of atherosclerosis. MicroRNAs (miRs) are regulators of inflammation and atherogenesis. The expressions of endothelial cell (EC)-specific miR-10a and miR-21 and monocyte-specific miR-33a and miR-221 were investigated using coculture of the ECs and monocytes upon exposure to H2O2 as an oxidative stressor, and endotoxin/lipopolysaccharide (LPS) as a microbial stressor. Human umbilical endothelial cells (HUVECs) and peripheral blood mononuclear cells (or monocytes) were cocultured in M199 complete medium and were incubated with LPS (20 ng/mL) or H2O2 (1%) for 8 hours at 37°C. The HUVECs and monocytes were then separated from the cellular mix using a magnetic bead negative selection technique. The relative expression of miRs was determined by real-time polymerase chain reaction. In both cell types, H2O2 induced miR10a ( P = 0.05) and LPS induced miR21 ( P = 0.0003) compared to the untreated controls. Coculture increased miR-10a and miR-21 expression in monocytes ( P = 0.0008 and <0.0001); however when cultured alone, HUVECs expressed higher levels of miR-10a and miR-21 ( P < 0.0001 and <0.0001). Coculture decreased the expression of miR-33a in monocytes ( P < 0.0001) while increasing miR221 in HUVECs and monocytes ( P < 0.0001 and <0.0001). The expression pattern of miRs in HUVECs and monocytes changes in the coculture compared to culturing alone in response to oxidative and microbial toxic compounds. Moreover, different cellular stressors induce different athero-miRs, which may affect the course of inflammation.


Assuntos
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Peróxido de Hidrogênio/toxicidade , Lipopolissacarídeos/toxicidade , MicroRNAs/metabolismo , Monócitos/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Células Cultivadas , Técnicas de Cocultura , Feminino , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Masculino , Monócitos/metabolismo
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