scholarly journals Metabolite Transporters as Regulators of Immunity

Metabolites ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 418
Author(s):  
Hauke J. Weiss ◽  
Stefano Angiari
Keyword(s):  
Intracellular Signaling ◽  
Cell Function ◽  
Immune Cell ◽  
Innate Immune ◽  
Signaling Cascades ◽  
Effector Functions ◽  
Immunological Responses ◽  
The Face ◽  
Specific Receptors

In the past decade, the rise of immunometabolism has fundamentally reshaped the face of immunology. As the functions and properties of many (immuno)metabolites have now been well described, their exchange among cells and their environment have only recently sparked the interest of immunologists. While many metabolites bind specific receptors to induce signaling cascades, some are actively exchanged between cells to communicate, or induce metabolic reprograming. In this review, we give an overview about how active metabolite transport impacts immune cell function and shapes immunological responses. We present some examples of how specific transporters feed into metabolic pathways and initiate intracellular signaling events in immune cells. In particular, we focus on the role of metabolite transporters in the activation and effector functions of T cells and macrophages, as prototype adaptive and innate immune cell populations.

scholarly journals Critical Role of Zinc Transporter (ZIP8) in Myeloid Innate Immune Cell Function and the Host Response against Bacterial Pneumonia

2021 ◽  
pp. ji2001395
Author(s):  
Sannette C. Hall ◽  
Deandra R. Smith ◽  
Shetty Ravi Dyavar ◽  
Todd A. Wyatt ◽  
Derrick R. Samuelson ◽  
...  
Keyword(s):  
Host Response ◽  
Bacterial Pneumonia ◽  
Cell Function ◽  
Immune Cell ◽  
Critical Role ◽  
Zinc Transporter ◽  
Innate Immune ◽  
Innate Immune Cell ◽  
Immune Cell Function

Regulatory role of periodontal ligament fibroblasts for innate immune cell function and differentiation

2012 ◽  
Vol 18 (5) ◽  
pp. 745-752 ◽  
Author(s):  
Anna Konermann ◽  
Dirk Stabenow ◽  
Percy A Knolle ◽  
Stefanie AE Held ◽  
James Deschner ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Cell Function ◽  
Immune Cell ◽  
Innate Immune ◽  
Innate Immune Cell ◽  
Regulatory Role ◽  
Immune Cell Function ◽  
Periodontal Ligament Fibroblasts

Immunology and cytokine pathways

2018 ◽  
Author(s):  
Bruce Kirkham
Keyword(s):  
Psoriatic Arthritis ◽  
Immune Cells ◽  
Cell Function ◽  
Immune Cell ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
New Information ◽  
Key Pathways

Psoriatic arthritis immunopathology has become the subject of intense study. These findings show differences to other forms of inflammatory arthritis in key pathways. Increased knowledge of innate immunity and the important role of IL-17/23 biology in both psoriasis and psoriatic arthritis, have led to new theories of immunopathogenesis in both conditions. Direct environmental stimuli could trigger innate immune cells resident in skin, which may then initiate a chronic adaptive immune response. The joint has fewer resident innate immune cells, but new studies show cells producing IL-17 may play key roles in immunopathology. The new information summarized here will provide important hypotheses for investigation of pathogenic pathways. Differences in non-immune cell function may also be critical mediators of response, for example, production of IL-12 or IL-23 by dendritic cells. Keratinocytes in skin and fibroblasts in joints may be critical in mediating cytokine production and effector function.

scholarly journals The Role of TRPV4 in Regulating Innate Immune Cell Function in Lung Inflammation

2020 ◽  
Vol 11 ◽  
Author(s):  
Rachel G. Scheraga ◽  
Brian D. Southern ◽  
Lisa M. Grove ◽  
Mitchell A. Olman
Keyword(s):  
Lung Inflammation ◽  
Cell Function ◽  
Immune Cell ◽  
Innate Immune ◽  
Innate Immune Cell ◽  
Immune Cell Function

Liver cell hydration and integrin signaling

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Michele Bonus ◽  
Dieter Häussinger ◽  
Holger Gohlke
Keyword(s):  
Cell Volume ◽  
Liver Cell ◽  
Cell Function ◽  
The Other ◽  
Signaling Cascades ◽  
Integrin Signaling ◽  
Volume Changes ◽  
The One ◽  
And Oxidative Stress

Abstract Liver cell hydration (cell volume) is dynamic and can change within minutes under the influence of hormones, nutrients, and oxidative stress. Such volume changes were identified as a novel and important modulator of cell function. It provides an early example for the interaction between a physical parameter (cell volume) on the one hand and metabolism, transport, and gene expression on the other. Such events involve mechanotransduction (osmosensing) which triggers signaling cascades towards liver function (osmosignaling). This article reviews our own work on this topic with emphasis on the role of β1 integrins as (osmo-)mechanosensors in the liver, but also on their role in bile acid signaling.

scholarly journals MMP-19 deficiency causes aggravation of colitis due to defects in innate immune cell function

2015 ◽  
Vol 9 (4) ◽  
pp. 974-985 ◽  
Author(s):  
R Brauer ◽  
J Tureckova ◽  
I Kanchev ◽  
M Khoylou ◽  
J Skarda ◽  
...  
Keyword(s):  
Cell Function ◽  
Immune Cell ◽  
Innate Immune ◽  
Innate Immune Cell ◽  
Immune Cell Function

scholarly journals Deletion of cftr leads to an excessive neutrophilic response and defective tissue repair in a zebrafish model of sterile inflammation

2019 ◽  
Author(s):  
Audrey Bernut ◽  
Catherine A. Loynes ◽  
R. Andres Floto ◽  
Stephen A. Renshaw
Keyword(s):  
Cystic Fibrosis ◽  
Tissue Repair ◽  
Cell Function ◽  
Immune Cell ◽  
Genetic Disorder ◽  
Innate Immune ◽  
Lung Damage ◽  
Tanshinone Iia ◽  
Sterile Inflammation ◽  
Inflammatory Status

AbstractInflammation-related progressive lung destruction is the leading causes of premature death in cystic fibrosis (CF), a genetic disorder caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. However, therapeutic targeting of inflammation has been hampered by a lack of understanding of the links between a dysfunctional CFTR and the deleterious innate immune response in CF. Herein, we used CFTR-depleted zebrafish larvae as an innovative in vivo vertebrate model, mimicking aspects of the inflammatory pathology of CF-related lung, to understand how CFTR dysfunction leads to abnormal inflammatory status in CF.We show that impaired CFTR-mediated inflammation correlates with an exuberant neutrophilic response after injury: CF zebrafish exhibit enhanced and sustained accumulation of neutrophils at wounds. Excessive epithelial oxidative responses drive enhanced neutrophil recruitment towards wounds. Persistence of neutrophils at inflamed sites is associated with impaired reverse migration of neutrophils and reduction in neutrophil apoptosis. As a consequence, the increased number of neutrophils at wound sites causes tissue damage and abnormal tissue repair. Importantly, the pro-resolution molecule Tanshinone IIA successfully re-balances inflammation both by accelerating inflammation resolution and by improving tissue repair in CFTR-deficient animal.Larval zebrafish giving a unique insight into innate immune cell function in CFTR deficiency, our findings bring important new understanding of the mechanisms underlying the inflammatory pathology in CF, which could be addressed therapeutically to prevent inflammatory lung damage in CF patients with potential improvements in disease outcomes.

The complex role of EZH2 in the tumor microenvironment: opportunities and challenges for immunotherapy combinations

2020 ◽  
Vol 12 (15) ◽  
pp. 1415-1430
Author(s):  
Jing Qiu ◽  
Shikhar Sharma ◽  
Robert A Rollins ◽  
Thomas A Paul
Keyword(s):  
Tumor Microenvironment ◽  
Cell Fate ◽  
Cell Function ◽  
Immune Dysfunction ◽  
Lymphoid Cells ◽  
Epigenetic Changes ◽  
Immune Effector ◽  
Effector Functions ◽  
Tumor Immunogenicity

Immune dysfunction in the tumor microenvironment occurs through epigenetic changes in both tumor cells and immune cells that alter transcriptional programs driving cell fate and cell function. Oncogenic activation of the histone methyltransferase EZH2 mediates gene expression changes, governing tumor immunogenicity as well as differentiation, survival and activation states of immune lineages. Emerging preclinical studies have highlighted the potential for EZH2 inhibitors to reverse epigenetic immune suppression in tumors and combine with immune checkpoint therapies. However, EZH2 activity is essential for the development of lymphoid cells, performing critical immune effector functions within tumors. In this review, we highlight the complexity of EZH2 function in immune regulation which may impact the implementation of combination with immunotherapy agents in clinic.

scholarly journals Myeloperoxidase Modulates Hydrogen Peroxide Mediated Cellular Damage in Murine Macrophages

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1255
Author(s):  
Chaorui Guo ◽  
Inga Sileikaite ◽  
Michael J. Davies ◽  
Clare L. Hawkins
Keyword(s):  
Hydrogen Peroxide ◽  
Hypochlorous Acid ◽  
Cell Function ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Cellular Damage ◽  
Enzymatic System ◽  
Therapeutic Approaches ◽  
Macrophage Cell

Myeloperoxidase (MPO) is involved in the development of many chronic inflammatory diseases, in addition to its key role in innate immune defenses. This is attributed to the excessive production of hypochlorous acid (HOCl) by MPO at inflammatory sites, which causes tissue damage. This has sparked wide interest in the development of therapeutic approaches to prevent HOCl-induced cellular damage including supplementation with thiocyanate (SCN−) as an alternative substrate for MPO. In this study, we used an enzymatic system composed of glucose oxidase (GO), glucose, and MPO in the absence and presence of SCN−, to investigate the effects of generating a continuous flux of oxidants on macrophage cell function. Our studies show the generation of hydrogen peroxide (H2O2) by glucose and GO results in a dose- and time-dependent decrease in metabolic activity and cell viability, and the activation of stress-related signaling pathways. Interestingly, these damaging effects were attenuated by the addition of MPO to form HOCl. Supplementation with SCN−, which favors the formation of hypothiocyanous acid, could reverse this effect. Addition of MPO also resulted in upregulation of the antioxidant gene, NAD(P)H:quinone acceptor oxidoreductase 1. This study provides new insights into the role of MPO in the modulation of macrophage function, which may be relevant to inflammatory pathologies.

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