scholarly journals Rac GTPase Signaling in Immune-Mediated Mechanisms of Atherosclerosis

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2808
Author(s):  
Cadence F. Lee ◽  
Rachel E. Carley ◽  
Celia A. Butler ◽  
Alan R. Morrison
Keyword(s):  
Treatment Strategies ◽  
Atherosclerotic Vascular Disease ◽  
Rac Gtpase ◽  
Immune Signaling ◽  
Adaptive Immune ◽  
Signaling Mechanisms ◽  
Immune Mediated ◽  
Artery Disease ◽  
Preclinical And Clinical Studies

Coronary artery disease caused by atherosclerosis is a major cause of morbidity and mortality around the world. Data from preclinical and clinical studies support the belief that atherosclerosis is an inflammatory disease that is mediated by innate and adaptive immune signaling mechanisms. This review sought to highlight the role of Rac-mediated inflammatory signaling in the mechanisms driving atherosclerotic calcification. In addition, current clinical treatment strategies that are related to targeting hypercholesterolemia as a critical risk factor for atherosclerotic vascular disease are addressed in relation to the effects on Rac immune signaling and the implications for the future of targeting immune responses in the treatment of calcific atherosclerosis.

scholarly journals Tuning cancer fate: the unremitting role of host immunity

Open Biology ◽  
2017 ◽  
Vol 7 (4) ◽  
pp. 170006 ◽  
Author(s):  
B. Calì ◽  
B. Molon ◽  
A. Viola
Keyword(s):  
Immune Cells ◽  
Immune Cell ◽  
Tumour Progression ◽  
Host Immunity ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
Immune Mediated ◽  
Immune Cell Subsets ◽  
Therapeutic Protocols

Host immunity plays a central and complex role in dictating tumour progression. Solid tumours are commonly infiltrated by a large number of immune cells that dynamically interact with the surrounding microenvironment. At first, innate and adaptive immune cells successfully cooperate to eradicate microcolonies of transformed cells. Concomitantly, surviving tumour clones start to proliferate and harness immune responses by specifically hijacking anti-tumour effector mechanisms and fostering the accumulation of immunosuppressive immune cell subsets at the tumour site. This pliable interplay between immune and malignant cells is a relentless process that has been concisely organized in three different phases: elimination, equilibrium and escape. In this review, we aim to depict the distinct immune cell subsets and immune-mediated responses characterizing the tumour landscape throughout the three interconnected phases. Importantly, the identification of key immune players and molecules involved in the dynamic crosstalk between tumour and immune system has been crucial for the introduction of reliable prognostic factors and effective therapeutic protocols against cancers.

scholarly journals Genetic and Epigenetic Aspects of Atopic Dermatitis

2020 ◽  
Vol 21 (18) ◽  
pp. 6484 ◽  
Author(s):  
Bogusław Nedoszytko ◽  
Edyta Reszka ◽  
Danuta Gutowska-Owsiak ◽  
Magdalena Trzeciak ◽  
Magdalena Lange ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Treatment Strategies ◽  
Structural Proteins ◽  
Epigenetic Changes ◽  
Epigenetic Alterations ◽  
Adaptive Immune ◽  
Genes Encoding ◽  
Inflammatory Processes ◽  
Non Coding Rnas

Atopic dermatitis is a heterogeneous disease, in which the pathogenesis is associated with mutations in genes encoding epidermal structural proteins, barrier enzymes, and their inhibitors; the role of genes regulating innate and adaptive immune responses and environmental factors inducing the disease is also noted. Recent studies point to the key role of epigenetic changes in the development of the disease. Epigenetic modifications are mainly mediated by DNA methylation, histone acetylation, and the action of specific non-coding RNAs. It has been documented that the profile of epigenetic changes in patients with atopic dermatitis (AD) differs from that observed in healthy people. This applies to the genes affecting the regulation of immune response and inflammatory processes, e.g., both affecting Th1 bias and promoting Th2 responses and the genes of innate immunity, as well as those encoding the structural proteins of the epidermis. Understanding of the epigenetic alterations is therefore pivotal to both create new molecular classifications of atopic dermatitis and to enable the development of personalized treatment strategies.

Hypertension

2021 ◽  
pp. 43-61
Keyword(s):  
Renal Disease ◽  
Renal Artery ◽  
Treatment Options ◽  
Treatment Strategies ◽  
Western World ◽  
Interventional Treatment ◽  
Lifestyle Modifications ◽  
Artery Disease ◽  
Progressive Renal Disease

Hypertension (HTN) is a common condition and a risk factor for numerous comorbidities, including cardiovascular disease, cerebrovascular disease, and progressive renal disease. In many people the aetiology of HTN is unknown, but in some a triggering “secondary” cause can be identified, e.g. renal disease, endocrine, or other underlying condition. For most people the treatment of HTN is straightforward, but in a small number the blood pressure can become “malignant or accelerated” and require urgent treatment or hospitalization. The chapters in this section provide an overview of the clinical assessment and investigation of a hypertensive patient, the recommended lifestyle modifications and pharmacological treatment options available, and potential complications of HTN. Renal artery stenosis a common cause of HTN that can be caused by atheromatous renovascular disease (ARVD) or other rarer pathologies, including fibromuscular disease, Takayasu’s arteritis, or other syndromes. ARVD is the commonest cause of renal artery disease in the Western world and in this section the authors focus upon the epidemiology and clinical presentation of ARVD and the potential diagnostic and treatment strategies. A particular focus is given to the role of medical and interventional treatment of ARVD, including potential outcomes, complications, and prognosis.

scholarly journals The Role of Sex Hormones in Multiple Sclerosis

2018 ◽  
Vol 80 (1-2) ◽  
pp. 93-99 ◽  
Author(s):  
Mirla Avila ◽  
Arpana Bansal ◽  
John Culberson ◽  
Alan N. Peiris
Keyword(s):  
Multiple Sclerosis ◽  
Sex Hormones ◽  
Treatment Strategies ◽  
Female Gender ◽  
Current Treatment ◽  
Sex Hormone ◽  
Immune Mediated ◽  
Autoimmune Conditions ◽  
The Central Nervous System

Multiple sclerosis (MS) is a chronic inflammatory demyelination disorder with an immune-mediated pathophysiology that affects the central nervous system (CNS). Like other autoimmune conditions, it has a predilection for female gender. This suggests a gender bias and a possible hormonal association. Inflammation and demyelination are hallmarks of MS. Oligodendrocytes are the myelinating cells of the CNS and these continue to be generated by oligodendrocyte precursor cells (OPCs). The process of remyelination represents a major form of plasticity in the developing adult CNS. Remyelination does occur in MS, but the process is largely inadequate and/or incomplete. Current treatment strategies primarily focus on reducing inflammation or immunosuppression, but there is a need for more extensive research on re-myelination as a possible mechanism of treatment. Previous studies have shown that pregnancy leads to an increase in OPC proliferation, oligodendrocyte generation and the number of myelinated axons in the maternal CNS. Studies have also suggested that this remyelination is possibly mediated by estriol. Sex hormones in particular have been shown to have an immuno-protective effect in TH1-driven autoimmunity diseases. The aim of our article is to review the available research on sex hormone-specific immune modulatory effects, assess its remyelination potential in MS, and suggest a future path for more extensive research on sex hormone as a target for therapeutics in MS.

scholarly journals Adaptive Immune Responses in Primary Cutaneous Sarcoidosis

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Matteo Bordignon ◽  
Paola Rottoli ◽  
Carlo Agostini ◽  
Mauro Alaibac
Keyword(s):  
Dendritic Cells ◽  
Treatment Strategies ◽  
Immunological Response ◽  
Inflammatory Disorder ◽  
Cutaneous Sarcoidosis ◽  
Cutaneous Lesions ◽  
Adaptive Immune ◽  
Immunological Mechanisms ◽  
Adaptive Immune Systems

Sarcoidosis is a multisystemic inflammatory disorder with cutaneous lesions present in about one-quarter of the patients. Cutaneous lesions have been classified as specific and nonspecific, depending on the presence of nonnecrotizing epithelial cell granulomas on histologic studies. The development and progression of specific cutaneous sarcoidosis involves a complex interaction between cells of the adaptive immune systems, notably T-lymphocytes and dendritic cells. In this paper, we will discuss the role of T-cells and skin dendritic cells in the development of primary cutaneous sarcoidosis and comment on the potential antigenic stimuli that may account for the development of the immunological response. We will further explore the contributions of selected cytokines to the immunopathological process. The knowledge of the adaptive immunological mechanisms operative in cutaneous sarcoidosis may subsequently be useful for identifying prevention and treatment strategies of systemic sarcoidosis.

scholarly journals Modulating Neuroinflammation to Treat Neuropsychiatric Disorders

2017 ◽  
Vol 2017 ◽  
pp. 1-21 ◽  
Author(s):  
Franziska A. Radtke ◽  
Gareth Chapman ◽  
Jeremy Hall ◽  
Yasir A. Syed
Keyword(s):  
Psychiatric Disorders ◽  
Cognitive Deficits ◽  
Inflammatory Responses ◽  
Copy Number Variants ◽  
Treatment Strategies ◽  
Behavioral Responses ◽  
Neuropsychiatric Disorders ◽  
Current Therapies ◽  
Preclinical And Clinical Studies

Neuroinflammation is recognised as one of the potential mechanisms mediating the onset of a broad range of psychiatric disorders and may contribute to nonresponsiveness to current therapies. Both preclinical and clinical studies have indicated that aberrant inflammatory responses can result in altered behavioral responses and cognitive deficits. In this review, we discuss the role of inflammation in the pathogenesis of neuropsychiatric disorders and ask the question if certain genetic copy-number variants (CNVs) associated with psychiatric disorders might play a role in modulating inflammation. Furthermore, we detail some of the potential treatment strategies for psychiatric disorders that may operate by altering inflammatory responses.

scholarly journals Peptide presentation by HLA-DQ molecules is associated with the development of immune tolerance

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5118 ◽  
Author(s):  
Máté Manczinger ◽  
Lajos Kemény
Keyword(s):  
Autoimmune Diseases ◽  
Immune Tolerance ◽  
Special Role ◽  
Immune Recognition ◽  
Adaptive Immune ◽  
Immune Mediated ◽  
Hla Dq ◽  
Human Proteins ◽  
Epitope Binding

HLA class II proteins are important elements of human adaptive immune recognition and are associated with numerous infectious and immune-mediated diseases. These highly variable molecules can be classified into DP, DQ and DR groups. It has been proposed that in contrast with DP and DR, epitope binding by DQ variants rather results in immune tolerance. However, the pieces of evidence are limited and controversial. We found that DQ molecules bind more human epitopes than DR. Pathogen-associated epitopes bound by DQ molecules are more similar to human proteins than the ones bound by DR. Accordingly, DQ molecules bind epitopes of significantly different pathogen species. Moreover, the binding of autoimmunity-associated epitopes by DQ confers protection from autoimmune diseases. Our results suggest a special role of HLA-DQ in immune homeostasis and help to better understand the association of HLA molecules with infectious and autoimmune diseases.

scholarly journals Emerging Roles for the Gut Microbiome in Lymphoid Neoplasms

2021 ◽  
Vol 15 ◽  
pp. 117955492110241
Author(s):  
Zhuangzhuang Shi ◽  
Mingzhi Zhang
Keyword(s):  
Gut Microbiota ◽  
Gut Microbiome ◽  
Disease Burden ◽  
Molecular Mechanisms ◽  
Treatment Strategies ◽  
Physiological Processes ◽  
Lymphoid Neoplasms ◽  
Promising Target ◽  
Preclinical And Clinical Studies

Lymphoid neoplasms encompass a heterogeneous group of malignancies with a predilection for immunocompromised individuals, and the disease burden of lymphoid neoplasms has been rising globally over the last decade. At the same time, mounting studies delineated a crucial role of the gut microbiome in the aetiopathogenesis of various diseases. Orchestrated interactions between myriad microorganisms and the gastrointestinal mucosa establish a defensive barrier for a range of physiological processes, especially immunity and metabolism. These findings provide new perspectives to harness our knowledge of the gut microbiota for preclinical and clinical studies of lymphoma. Here, we review recent findings that support a role for the gut microbiota in the development of lymphoid neoplasms and pinpoint relevant molecular mechanisms. Accordingly, we propose the microbiota-gut-lymphoma axis as a promising target for clinical translation, including auxiliary diagnosis, novel prevention and treatment strategies, and predicting clinical outcomes and treatment-related adverse effects of the disease in the future. This review will reveal a fascinating avenue of research in the microbiota-mediated lymphoma field.

scholarly journals Human IL-23R Cytokine-Binding Homology Region-Fc Fusion Protein Ameliorates Psoriasis via the Decrease of Systemic Th17 and ILC3 Cell Responses

2019 ◽  
Vol 20 (17) ◽  
pp. 4170 ◽  
Author(s):  
Yue Gao ◽  
Zhengying Bian ◽  
Wenyao Xue ◽  
Qianwen Li ◽  
Yu Zeng ◽  
...  
Keyword(s):  
Fusion Protein ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Inflammatory Factors ◽  
Cell Responses ◽  
Adaptive Immune ◽  
Immune Mediated ◽  
Fc Fusion Protein ◽  
Shed Light

Interleukin (IL)-23 is considered an effective therapeutic target for the treatment of psoriasis because of the crucial role of the IL-23/IL-17 axis in the pathogenesis of psoriasis, and it has recently been reported to be involved in ILC3 cell differentiation. In this study, we report that eukaryotically expressed rhIL23R-CHR/Fc, as an endogenous extracellular receptor analogue, could be a natural antagonist in an imiquimod (IMQ)-induced psoriasis-like mouse model, including the antagonizing effect of suppressed inflammation in the skin lesion, decreased production of pro-inflammatory cells, and reduced the expression of pro-inflammatory factors. The rhIL23R-CHR/Fc fusion protein inhibits both innate immune and adaptive immune-mediated inflammatory responses. These findings shed light on rhIL23R-CHR/Fc as a promising candidate therapy for the treatment of psoriasis.

Post-stroke recrudescence—a possible connection to autoimmunity?

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Yosuke Akamatsu ◽  
Hersh J. Chaitin ◽  
Khalid A. Hanafy
Keyword(s):  
Acute Infection ◽  
Adaptive Immune System ◽  
Underlying Mechanism ◽  
Stroke Outcome ◽  
Post Stroke ◽  
Adaptive Immune ◽  
Immune Mediated ◽  
Clinical Models

Abstract Early recanalization of the occluded vessel is the only efficient intervention that improves outcome after ischemic stroke. In contrast, interventions for chronic issues facing stroke patients are limited. Recent clinical and preclinical studies have shown a correlation between upregulated immune responses to brain antigens and post-stroke recrudescence (PSR), post-stroke fatigue (PSF), and dementia (PSD); all of which are associated with poor long-term stroke outcome. Recent retrospective studies have demonstrated a strong correlation between the onset of PSR and acute infection during acute stroke, suggesting some adaptive immune system mediated pathology. This review will discuss the mechanisms and epidemiology of PSR based on the current clinical and pre-clinical evidence. Accordingly, PSR does appear correlated with populations that are prone to autoimmunity, infection, and subsequent triggers, which corroborate autoimmune responses to self-brain antigens as an underlying mechanism. Moreover, PSR as well as PSF and PSD seem to be partly explained by the development of a neuro-inflammatory response to brain antigens. Therefore, the future of improving long-term stroke outcome could be bright with more accurate pre-clinical models focusing on the role of adaptive immune-mediated post stroke neuroinflammation and more clinical studies of PSR.

Sign in / Sign up

Export Citation Format

Share Document