The Role of Interleukin-27 in Atherosclerosis: A Contemporary Review

Cardiology ◽  
2021 ◽  
pp. 1-13
Author(s):  
Mehrian Jafarizade ◽  
Farima Kahe ◽  
Sadaf Sharfaei ◽  
Kaveh Momenzadeh ◽  
Anmol Pitliya ◽  
...  
Keyword(s):  
Vascular Endothelium ◽  
Inflammatory Diseases ◽  
Atherosclerotic Plaques ◽  
Future Studies ◽  
Coronary Syndrome ◽  
Autoimmune And Inflammatory Diseases ◽  
Biologic Function ◽  
Definite Role ◽  
Inflammatory System

Atherosclerosis is a chronic inflammation characterized by an imbalance between inhibitors and stimulators of the inflammatory system that leads to the formation of atherosclerotic plaques in the vessel walls. Interleukin (IL)-27 is one of the recently discovered cytokines that have an immunomodulatory role in autoimmune and inflammatory diseases. However, the definite role of IL-27 in the pathogenesis of atherosclerosis remains unclear. Recent studies on cardiomyocytes and vascular endothelium have demonstrated mechanisms through which IL-27 could potentially modulate atherosclerosis. Upregulation of the IL-27 receptor was also observed in the atherosclerotic plaques. In addition, circulatory IL-27 levels were increased in patients with acute coronary syndrome and myocardial infarction. A regenerative, neovascularization, and cardioprotective role of IL-27 has also been implicated. Future studies are warranted to elucidate the biologic function and clinical significance of IL-27 in atherosclerosis.

scholarly journals The Pathophysiological Role of Neutrophil Extracellular Traps in Inflammatory Diseases

2018 ◽  
Vol 118 (01) ◽  
pp. 006-027 ◽  
Author(s):  
Aldo Bonaventura ◽  
Luca Liberale ◽  
Federico Carbone ◽  
Alessandra Vecchié ◽  
Candela Diaz-Cañestro ◽  
...  
Keyword(s):  
Serine Proteases ◽  
Inflammatory Diseases ◽  
Vascular Diseases ◽  
Neutrophil Extracellular Traps ◽  
Human Beings ◽  
Coronary Syndrome ◽  
Extracellular Traps ◽  
Atherosclerotic Lesions ◽  
Autoimmune And Inflammatory Diseases

AbstractNeutrophil pathogen-killing mechanism termed neutrophil extracellular traps (NETs) has been recently identified. NETs consist of chromatin and histones along with serine proteases and myeloperoxidase and are induced by a great variety of infectious and non-infectious stimuli. NETosis is a kind of programmed neutrophil death characterized by chromatin decondensation and release of nuclear granular contents, mainly driven by peptidylarginine deiminase 4 citrullination of histones. Although classically related to the protection against infectious pathogens, nowadays NETs have been described as a player of several pathophysiological processes. Neutrophil dysregulation has been demonstrated in the pathogenesis of most representative vascular diseases, such as acute coronary syndrome, stroke and venous thrombosis. Indeed, NETs have been identified within atherosclerotic lesions and arterial thrombi in both human beings and animal models. Moreover, an imbalance in this mechanism has been proposed as a critical source of modified and/or externalized autoantigens in autoimmune and inflammatory diseases. Finally, an update on the role of NETs in the pathogenesis of cancer has been included. In the present review, based on papers released on PubMed and MEDLINE up to July 2017, we point to update the knowledge on NETs, from their structure to their roles in infectious diseases as well as in cardiovascular diseases, autoimmunity, metabolic disorders and cancer, with a look to future perspectives and therapeutic opportunities.

Lymphocyte signaling and activation by the CARMA1-BCL10-MALT1 signalosome

2016 ◽  
Vol 397 (12) ◽  
pp. 1315-1333 ◽  
Author(s):  
Isabel Meininger ◽  
Daniel Krappmann
Keyword(s):  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Critical Role ◽  
Antigen Receptor ◽  
Lymphocyte Activation ◽  
Downstream Signaling ◽  
Antigen Receptor Signaling ◽  
Autoimmune And Inflammatory Diseases ◽  
And Function

Abstract The CARMA1-BCL10-MALT1 (CBM) signalosome triggers canonical NF-κB signaling and lymphocyte activation upon antigen-receptor stimulation. Genetic studies in mice and the analysis of human immune pathologies unveiled a critical role of the CBM complex in adaptive immune responses. Great progress has been made in elucidating the fundamental mechanisms that dictate CBM assembly and disassembly. By bridging proximal antigen-receptor signaling to downstream signaling pathways, the CBM complex exerts a crucial scaffolding function. Moreover, the MALT1 subunit confers a unique proteolytic activity that is key for lymphocyte activation. Deregulated ‘chronic’ CBM signaling drives constitutive NF-κB signaling and MALT1 activation, which contribute to the development of autoimmune and inflammatory diseases as well as lymphomagenesis. Thus, the processes that govern CBM activation and function are promising targets for the treatment of immune disorders. Here, we summarize the current knowledge on the functions and mechanisms of CBM signaling in lymphocytes and how CBM deregulations contribute to aberrant signaling in malignant lymphomas.

scholarly journals Genetic perturbation of PU.1 binding and chromatin looping at neutrophil enhancers associates with autoimmune disease

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Stephen Watt ◽  
Louella Vasquez ◽  
Klaudia Walter ◽  
Alice L. Mann ◽  
Kousik Kundu ◽  
...  
Keyword(s):  
Transcriptional Control ◽  
Disease Susceptibility ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Genetic Associations ◽  
Functional Interpretation ◽  
Autoimmune And Inflammatory Diseases ◽  
Immune Traits ◽  
Downstream Gene Expression

AbstractNeutrophils play fundamental roles in innate immune response, shape adaptive immunity, and are a potentially causal cell type underpinning genetic associations with immune system traits and diseases. Here, we profile the binding of myeloid master regulator PU.1 in primary neutrophils across nearly a hundred volunteers. We show that variants associated with differential PU.1 binding underlie genetically-driven differences in cell count and susceptibility to autoimmune and inflammatory diseases. We integrate these results with other multi-individual genomic readouts, revealing coordinated effects of PU.1 binding variants on the local chromatin state, enhancer-promoter contacts and downstream gene expression, and providing a functional interpretation for 27 genes underlying immune traits. Collectively, these results demonstrate the functional role of PU.1 and its target enhancers in neutrophil transcriptional control and immune disease susceptibility.

scholarly journals The Kynurenine Pathway—New Linkage between Innate and Adaptive Immunity in Autoimmune Endocrinopathies

2021 ◽  
Vol 22 (18) ◽  
pp. 9879
Author(s):  
Anna Krupa ◽  
Irina Kowalska
Keyword(s):  
Immune System ◽  
Adaptive Immunity ◽  
Immune Cells ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Kynurenine Pathway ◽  
Wide Range ◽  
Organ Specific ◽  
Autoimmune And Inflammatory Diseases

The kynurenine pathway (KP) is highly regulated in the immune system, where it promotes immunosuppression in response to infection or inflammation. Indoleamine 2,3-dioxygenase 1 (IDO1), the main enzyme of KP, has a broad spectrum of activity on immune cells regulation, controlling the balance between stimulation and suppression of the immune system at sites of local inflammation, relevant to a wide range of autoimmune and inflammatory diseases. Various autoimmune diseases, among them endocrinopathies, have been identified to date, but despite significant progress in their diagnosis and treatment, they are still associated with significant complications, morbidity, and mortality. The precise cellular and molecular mechanisms leading to the onset and development of autoimmune disease remain poorly clarified so far. In breaking of tolerance, the cells of the innate immunity provide a decisive microenvironment that regulates immune cells’ differentiation, leading to activation of adaptive immunity. The current review provided a comprehensive presentation of the known role of IDO1 and KP activation in the regulation of the innate and adaptive arms of the immune system. Significant attention has been paid to the immunoregulatory role of IDO1 in the most prevalent, organ-specific autoimmune endocrinopathies—type 1 diabetes mellitus (T1DM) and autoimmune thyroiditis.

The role of IL-17 and anti-IL-17 agents in the immunopathogenesis and management of autoimmune and inflammatory diseases

2021 ◽  
pp. 108402
Author(s):  
S.P. Déo-Gracias Berry ◽  
Camille Dossou ◽  
Ali Kashif ◽  
Niusha Sharifinejad ◽  
Gholamreza Azizi ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Autoimmune And Inflammatory Diseases

Pathogenic role of anti-endothelial cell antibodies in autoimmune rheumatic diseases

Lupus ◽  
2009 ◽  
Vol 18 (13) ◽  
pp. 1233-1238 ◽  
Author(s):  
DS Domiciano ◽  
JF Carvalho ◽  
Y. Shoenfeld
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Inflammatory Diseases ◽  
Endothelial Damage ◽  
Systemic Lupus Erythematous ◽  
Pathogenic Role ◽  
Autoimmune Rheumatic Diseases ◽  
Pathological Conditions ◽  
Autoimmune And Inflammatory Diseases

Anti-endothelial cells antibodies have been detected in numerous autoimmune and inflammatory diseases, including systemic lupus erythematous, rheumatoid arthritis, vasculitis and sarcoidosis. Anti-endothelial cells antibodies bind to endothelial cell antigens and induce endothelial damage. Their effects on the endothelial cell have been considered responsible, at least in part, by the vascular injury which occurs in these pathological conditions.

scholarly journals Regulatory T cells in acute and chronic kidney diseases

2018 ◽  
Vol 314 (5) ◽  
pp. F679-F698 ◽  
Author(s):  
Rahul Sharma ◽  
Gilbert R. Kinsey
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cell Activation ◽  
Cell Function ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Kidney Diseases ◽  
Peripheral Tolerance ◽  
Autoimmune And Inflammatory Diseases

Foxp3-expressing CD4+ regulatory T cells (Tregs) make up one subset of the helper T cells (Th) and are one of the major mechanisms of peripheral tolerance. Tregs prevent abnormal activation of the immune system throughout the lifespan, thus protecting from autoimmune and inflammatory diseases. Recent studies have elucidated the role of Tregs beyond autoimmunity. Tregs play important functions in controlling not only innate and adaptive immune cell activation, but also regulate nonimmune cell function during insults and injury. Inflammation contributes to a multitude of acute and chronic diseases affecting the kidneys. This review examines the role of Tregs in pathogenesis of renal inflammatory diseases and explores the approaches for enhancing Tregs for prevention and therapy of renal inflammation.

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