scholarly journals Immune cells as targets for cardioprotection: new players and novel therapeutic opportunities

2019 ◽  
Vol 115 (7) ◽  
pp. 1117-1130 ◽  
Author(s):  
Ioanna Andreadou ◽  
Hector A Cabrera-Fuentes ◽  
Yvan Devaux ◽  
Nikolaos G Frangogiannis ◽  
Stefan Frantz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Inflammatory Reaction ◽  
Immune Cells ◽  
Cell Response ◽  
Immune Cell ◽  
Left Ventricular ◽  
Lymphoid Cells ◽  
Inflammatory Phase ◽  
Anti Inflammatory ◽  
Immune Cell Response

Abstract New therapies are required to reduce myocardial infarct (MI) size and prevent the onset of heart failure in patients presenting with acute myocardial infarction (AMI), one of the leading causes of death and disability globally. In this regard, the immune cell response to AMI, which comprises an initial pro-inflammatory reaction followed by an anti-inflammatory phase, contributes to final MI size and post-AMI remodelling [changes in left ventricular (LV) size and function]. The transition between these two phases is critical in this regard, with a persistent and severe pro-inflammatory reaction leading to adverse LV remodelling and increased propensity for developing heart failure. In this review article, we provide an overview of the immune cells involved in orchestrating the complex and dynamic inflammatory response to AMI—these include neutrophils, monocytes/macrophages, and emerging players such as dendritic cells, lymphocytes, pericardial lymphoid cells, endothelial cells, and cardiac fibroblasts. We discuss potential reasons for past failures of anti-inflammatory cardioprotective therapies, and highlight new treatment targets for modulating the immune cell response to AMI, as a potential therapeutic strategy to improve clinical outcomes in AMI patients. This article is part of a Cardiovascular Research Spotlight Issue entitled ‘Cardioprotection Beyond the Cardiomyocyte’, and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.

scholarly journals The Immunomodulatory and Anti-Inflammatory Effect of Curcumin on Immune Cell Populations, Cytokines, and In Vivo Models of Rheumatoid Arthritis

2021 ◽  
Vol 14 (4) ◽  
pp. 309
Author(s):  
Sebastian Makuch ◽  
Kamil Więcek ◽  
Marta Woźniak
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune Cells ◽  
Immune Cell ◽  
Autoimmune Disorder ◽  
Lymphoid Cells ◽  
In Vivo Models ◽  
Rheumatoid Arthritis Development ◽  
Bone Degradation ◽  
Anti Inflammatory

Rheumatoid arthritis (RA) is a widespread chronic autoimmune disorder affecting the joints, causing irreversible cartilage, synovium, and bone degradation. During the course of the disease, many immune and joint cells are activated, causing inflammation. Immune cells including macrophages, lymphocytes, neutrophils, mast cells, natural killer cells, innate lymphoid cells, as well as synovial tissue cells, like fibroblast-like synoviocytes, chondrocytes, and osteoclasts secrete different proinflammatory factors, including many cytokines, angiogenesis-stimulating molecules and others. Recent studies reveal that curcumin, a natural dietary anti-inflammatory compound, can modulate the response of the cells engaging in RA course. This review comprises detailed data about the pathogenesis and inflammation process in rheumatoid arthritis and demonstrates scientific investigations about the molecular interactions between curcumin and immune cells responsible for rheumatoid arthritis development to discuss this herbal drug’s immunoregulatory role in RA treatment.

scholarly journals Identification of Somatic Mutation-Driven Immune Cells by Integrating Genomic and Transcriptome Data

2021 ◽  
Vol 9 ◽  
Author(s):  
Ying Jiang ◽  
Baotong Zheng ◽  
Yang Yang ◽  
Xiangmei Li ◽  
Junwei Han
Keyword(s):  
Gene Mutation ◽  
Somatic Mutation ◽  
Immune Cells ◽  
Cell Response ◽  
Somatic Mutations ◽  
Immune Cell ◽  
Transcriptome Data ◽  
Mutation Status ◽  
Binary Matrices ◽  
Immune Cell Response

Tumor somatic mutations in protein-coding regions may generate neoantigens which may trigger antitumor immune cell response. Increasing evidence supports that immune cell response may profoundly influence tumor progression. However, there are no calculated tools to systematically identify immune cells driven by specific somatic mutations. It is urgent to develop a calculated method to comprehensively detect tumor-infiltrating immune cells driven by the specific somatic mutations in cancer. We developed a novel software package (SMDIC) that enables the automated identification of somatic mutation-driven immune cell. SMDIC provides a novel pipeline to discover mutation-specific immune cells by integrating genomic and transcriptome data. The operation modes include inference of the relative abundance matrix of tumor-infiltrating immune cells, detection of differential abundance immune cells with respect to the gene mutation status, conversion of the abundance matrix of significantly dysregulated cells into two binary matrices (one for upregulated and one for downregulated cells), identification of somatic mutation-driven immune cells by comparing the gene mutation status with each immune cell in the binary matrices across all samples, and visualization of immune cell abundance of samples in different mutation status for each gene. SMDIC provides a user-friendly tool to identify somatic mutation-specific immune cell response. SMDIC may contribute to understand the mechanisms underlying anticancer immune response and find targets for cancer immunotherapy. The SMDIC was implemented as an R-based tool which was freely available from the CRAN website https://CRAN.R-project.org/package=SMDIC.

scholarly journals RhoA Signaling in Immune Cell Response and Cardiac Disease

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1681
Author(s):  
Lucia Sophie Kilian ◽  
Derk Frank ◽  
Ashraf Yusuf Rangrez
Keyword(s):  
Cardiac Disease ◽  
Cell Response ◽  
Cell Activation ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Heart Diseases ◽  
Small Gtpase ◽  
Cardiac Inflammation ◽  
Immune Cell Activation ◽  
Immune Cell Response

Chronic inflammation, the activation of immune cells and their cross-talk with cardiomyocytes in the pathogenesis and progression of heart diseases has long been overlooked. However, with the latest research developments, it is increasingly accepted that a vicious cycle exists where cardiomyocytes release cardiocrine signaling molecules that spiral down to immune cell activation and chronic state of low-level inflammation. For example, cardiocrine molecules released from injured or stressed cardiomyocytes can stimulate macrophages, dendritic cells, neutrophils and even T-cells, which then subsequently increase cardiac inflammation by co-stimulation and positive feedback loops. One of the key proteins involved in stress-mediated cardiomyocyte signal transduction is a small GTPase RhoA. Importantly, the regulation of RhoA activation is critical for effective immune cell response and is being considered as one of the potential therapeutic targets in many immune-cell-mediated inflammatory diseases. In this review we provide an update on the role of RhoA at the juncture of immune cell activation, inflammation and cardiac disease.

scholarly journals IMMU-68. SINGLE-CELL PROTEOMIC ANALYSIS OF IMMUNE CELL RESPONSE TO CHECKPOINT BLOCKADE USING 30-PARAMETER FLOW CYTOMETRY

2018 ◽  
Vol 20 (suppl_6) ◽  
pp. vi137-vi137
Author(s):  
Amber Giles ◽  
Leonard Nettey ◽  
Thomas Liechti ◽  
Margaret Beddall ◽  
Elizabeth Vera ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Single Cell ◽  
Cell Response ◽  
Proteomic Analysis ◽  
Immune Cell ◽  
Checkpoint Blockade ◽  
Immune Cell Response

scholarly journals Postoperative cellular stress in the kidney is associated with an early systemic γδ T-cell immune cell response

Critical Care ◽  
2018 ◽  
Vol 22 (1) ◽  
Author(s):  
Ivan Göcze ◽  
Katharina Ehehalt ◽  
Florian Zeman ◽  
Paloma Riquelme ◽  
Karin Pfister ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Response ◽  
Immune Cell ◽  
Cellular Stress ◽  
Γδ T Cell ◽  
Immune Cell Response

Abstract 285: Cardiac Inflammation and Fibrosis Induced by Heart Failure Are Reversed by Short-Duration Estrogen Therapy

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Andrea Iorga ◽  
Rangarajan Nadadur ◽  
Salil Sharma ◽  
Jingyuan Li ◽  
Mansoureh Eghbali
Keyword(s):  
Heart Failure ◽  
Estrogen Therapy ◽  
Pressure Overload ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
In Vivo Model ◽  
Anti Inflammatory

Heart failure is generally characterized by increased fibrosis and inflammation, which leads to functional and contractile defects. We have previously shown that short-term estrogen (E2) treatment can rescue pressure overload-induced decompensated heart failure (HF) in mice. Here, we investigate the anti-inflammatory and anti-fibrotic effects of E2 on reversing the adverse remodeling of the left ventricle which occurs during the progression to heart failure. Trans-aortic constriction procedure was used to induce HF. Once the ejection fraction reached ∼30%, one group of mice was sacrificed and the other group was treated with E2 (30 αg/kg/day) for 10 days. In vitro, co-cultured neonatal rat ventricular myocytes and fibroblasts were treated with Angiotensin II (AngII) to simulate cardiac stress, both in the presence or absence of E2. In vivo RT-PCR showed that the transcript levels of the pro-fibrotic markers Collagen I, TGFβ, Fibrosin 1 (FBRS) and Lysil Oxidase (LOX) were significantly upregulated in HF (from 1.00±0.16 to 1.83±0.11 for Collagen 1, 1±0.86 to 4.33±0.59 for TGFβ, 1±0.52 to 3.61±0.22 for FBRS and 1.00±0.33 to 2.88±0.32 for LOX) and were reduced with E2 treatment to levels similar to CTRL. E2 also restored in vitro AngII-induced upregulation of LOX, TGFβ and Collagen 1 (LOX:1±0.23 in CTRL, 6.87±0.26 in AngII and 2.80±1.5 in AngII+E2; TGFβ: 1±0.08 in CTRL, 3.30±0.25 in AngII and 1.59±0.21 in AngII+E2; Collagen 1: 1±0.05 in CTRL.2±0.01 in AngII and 0.65±0.02 (p<0.05, values normalized to CTRL)). Furthermore, the pro-inflammatory interleukins IL-1β and IL-6 were upregulated from 1±0.19 to 1.90±0.09 and 1±0.30 to 5.29±0.77 in the in vivo model of HF, respectively, and reversed to CTRL levels with E2 therapy. In vitro, IL-1β was also significantly increased ∼ 4 fold from 1±0.63 in CTRL to 3.86±0.14 with AngII treatment and restored to 1.29±0.77 with Ang+E2 treatment. Lastly, the anti-inflammatory interleukin IL-10 was downregulated from 1.00±0.17 to 0.49±0.03 in HF and reversed to 0.67±0.09 in vivo with E2 therapy (all values normalized to CTRL). This data strongly suggests that one of the mechanisms for the beneficial action of estrogen on left ventricular heart failure is through reversal of inflammation and fibrosis.

Monocyte immune cell response and copper status in beef steers that grazed endophyte-infected tall fescue.

1998 ◽  
Vol 76 (10) ◽  
pp. 2694 ◽  
Author(s):  
K E Saker ◽  
V G Allen ◽  
J Kalnitsky ◽  
C D Thatcher ◽  
W S Swecker ◽  
...  
Keyword(s):  
Tall Fescue ◽  
Cell Response ◽  
Immune Cell ◽  
Beef Steers ◽  
Copper Status ◽  
Immune Cell Response ◽  
And Copper Status

scholarly journals Long Noncoding RNA in Myeloid and Lymphoid Cell Differentiation, Polarization and Function

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 269 ◽  
Author(s):  
Imran Ahmad ◽  
Araceli Valverde ◽  
Fayek Ahmad ◽  
Afsar Raza Naqvi
Keyword(s):  
Cell Differentiation ◽  
Immune Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Immune Cell ◽  
Lymphoid Cells ◽  
Tissue Cell ◽  
Specific Expression ◽  
And Function

Long noncoding RNA (lncRNA) are a class of endogenous, non-protein coding RNAs that are increasingly being associated with various cellular functions and diseases. Yet, despite their ubiquity and abundance, only a minute fraction of these molecules has an assigned function. LncRNAs show tissue-, cell-, and developmental stage-specific expression, and are differentially expressed under physiological or pathological conditions. The role of lncRNAs in the lineage commitment of immune cells and shaping immune responses is becoming evident. Myeloid cells and lymphoid cells are two major classes of immune systems that work in concert to initiate and amplify innate and adaptive immunity in vertebrates. In this review, we provide mechanistic roles of lncRNA through which these noncoding RNAs can directly participate in the differentiation, polarization, and activation of myeloid (monocyte, macrophage, and dendritic cells) and lymphoid cells (T cells, B cells, and NK cells). While our knowledge on the role of lncRNA in immune cell differentiation and function has improved in the past decade, further studies are required to unravel the biological role of lncRNAs and identify novel mechanisms of lncRNA functions in immune cells. Harnessing the regulatory potential of lncRNAs can provide novel diagnostic and therapeutic targets in treating immune cell related diseases.

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