scholarly journals CD39 as a marker of pathogenic CD8+ T cells in cancer and other chronic inflammatory diseases

Oncoscience ◽  
2018 ◽  
Vol 5 (3-4) ◽  
pp. 65-66 ◽  
Author(s):  
Fernando Pablo Canale ◽  
María Cecilia Ramello ◽  
Carolina Lucía Montes
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Inflammatory Diseases ◽  
Chronic Inflammatory Diseases

scholarly journals Alumina Ceramic Exacerbates the Inflammatory Disease by Activation of Macrophages and T Cells

2020 ◽  
Vol 21 (19) ◽  
pp. 7114
Author(s):  
Seong-Min Lim ◽  
Juyoung Hwang ◽  
Hae-Bin Park ◽  
Chan Ho Park ◽  
Jun-O Jin
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Fine Particles ◽  
Inflammatory Diseases ◽  
Artificial Joints ◽  
Al2o3 Ceramic ◽  
Adaptive Immune Cells ◽  
Materials Used

(1) Background: Aluminum oxide (Al2O3) ceramic is one of the materials used for artificial joints, and it has been known that their fine particles (FPs) are provided by the wear of the ceramic. Al2O3 FPs have been shown to induce macrophage activation in vitro; however, the inflammatory effect in vivo has not been studied. (2) Methods: We examined the in vivo effect of Al2O3 FPs on the innate and adaptive immune cells in the mice. (3) Results: Al2O3 FPs promoted the activation of spleen macrophages; however, conventional dendritic cells (cDCs), plasmacytoid DCs (pDCs), and natural killer (NK) cells were not activated. In addition, increases in the CD4 and CD8 T cells was induced in the spleens of the mice treated with Al2O3 FPs, which differentiated into interferon-gamma (IFN-γ)-producing helper T1 (Th1) and cytotoxic T1 (Tc1) cells. Finally, the injection of Al2O3 FPs exacerbated dextran sulfate sodium (DSS)-induced inflammation in the colon, mediated by activated and increased number of CD4 and CD8 T cells. (4) Conclusions: These data demonstrate that FPs of Al2O3 ceramic may contribute to the exacerbation of inflammatory diseases in the patients.

Calcium Signaling in T Cells and Chronic Inflammatory Disorders of the Oral Cavity

2021 ◽  
pp. 002203452199065
Author(s):  
S. Hasiakos ◽  
Y. Gwack ◽  
M. Kang ◽  
I. Nishimura
Keyword(s):  
T Cells ◽  
T Cell ◽  
Oral Cavity ◽  
Calcium Signaling ◽  
Signaling Pathways ◽  
Chronic Inflammation ◽  
Th17 Cells ◽  
Inflammatory Diseases ◽  
Chronic Inflammatory Diseases

Acute immune responses to microbial insults in the oral cavity often progress to chronic inflammatory diseases such as periodontitis and apical periodontitis. Chronic oral inflammation causes destruction of the periodontium, potentially leading to loss of the dentition. Previous investigations have demonstrated that the composition of oral immune cells, rather than the overall extent of cellular infiltration, determines the pathological development of chronic inflammation. The role of T lymphocyte populations, including Th1, Th2, Th17, and Treg cells, has been extensively described. Studies now propose pathogenic Th17 cells as a distinct subset, uniquely classifiable from traditional Th17 populations. In situ differentiation of pathogenic Th17 cells has been verified as a source of destructive inflammation, which critically drives pathogenesis in chronic inflammatory diseases such as diabetes, rheumatoid arthritis, and inflammatory bowel disease. Pathogenic Th17 cells resemble a Th1 penotype and produce not only interleukin 17 (IL-17) but also γ-interferon (IFN-γ) and granulocyte-macrophage colony-stimulating factor (GM-CSF). The proinflammatory cytokine-specific mechanisms known to induce IL-17 expression in Th17 cells are well characterized; however, differentiation mechanisms that lead to pathogenic Th17 cells are less understood. Recently, Ca2+ signaling through Ca2+ release-activated Ca2+ channels (CRAC) in T cells has been uncovered as a major signaling axis involved in the regulation of T-cell-mediated chronic inflammation. In particular, pathogenic Th17 cell–mediated immunological diseases appear to be effectively targeted via such Ca2+ signaling pathways. Pathogenic plasticity of Th17 cells has been extensively illustrated in autoimmune and chronic inflammatory diseases. Although their specific causal relationship to oral infection-induced chronic inflammatory diseases is not fully established, pathogenic Th17 cells may be involved in the underlining mechanism. This review highlights the current understanding of T-cell phenotype regulation, calcium signaling pathways in this event, and the potential role of pathogenic Th17 cells in chronic inflammatory disorders of the oral cavity.

scholarly journals Exploring inflammatory signatures in arthritic joint biopsies with Spatial Transcriptomics

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Konstantin Carlberg ◽  
Marina Korotkova ◽  
Ludvig Larsson ◽  
Anca I. Catrina ◽  
Patrik L. Ståhl ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Immune Cell ◽  
Memory T Cells ◽  
Inflammatory Diseases ◽  
Adaptive Immune Response ◽  
Cell Types ◽  
Effector Memory ◽  
Cellular Mechanisms ◽  
Chronic Inflammatory Diseases

AbstractLately it has become possible to analyze transcriptomic profiles in tissue sections with retained cellular context. We aimed to explore synovial biopsies from rheumatoid arthritis (RA) and spondyloarthritis (SpA) patients, using Spatial Transcriptomics (ST) as a proof of principle approach for unbiased mRNA studies at the site of inflammation in these chronic inflammatory diseases. Synovial tissue biopsies from affected joints were studied with ST. The transcriptome data was subjected to differential gene expression analysis (DEA), pathway analysis, immune cell type identification using Xcell analysis and validation with immunohistochemistry (IHC). The ST technology allows selective analyses on areas of interest, thus we analyzed morphologically distinct areas of mononuclear cell infiltrates. The top differentially expressed genes revealed an adaptive immune response profile and T-B cell interactions in RA, while in SpA, the profiles implicate functions associated with tissue repair. With spatially resolved gene expression data, overlaid on high-resolution histological images, we digitally portrayed pre-selected cell types in silico. The RA displayed an overrepresentation of central memory T cells, while in SpA effector memory T cells were most prominent. Consequently, ST allows for deeper understanding of cellular mechanisms and diversity in tissues from chronic inflammatory diseases.

Interleukin‐17 producing mucosal associated invariant T cells ‐ emerging players in chronic inflammatory diseases?

2020 ◽  
Vol 50 (8) ◽  
pp. 1098-1108 ◽  
Author(s):  
Marta M. Pisarska ◽  
Margaret R. Dunne ◽  
Donal O'Shea ◽  
Andrew E. Hogan
Keyword(s):  
T Cells ◽  
Inflammatory Diseases ◽  
Interleukin 17 ◽  
Chronic Inflammatory Diseases ◽  
Invariant T Cells

scholarly journals CD28null CD4 T-cell expansions in autoimmune disease suggest a link with cytomegalovirus infection

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 327 ◽  
Author(s):  
Aalia Bano ◽  
Alejandra Pera ◽  
Ahmad Almoukayed ◽  
Thomas H.S. Clarke ◽  
Sukaina Kirmani ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Cd4 T Cells ◽  
Cytomegalovirus Infection ◽  
Inflammatory Diseases ◽  
Cytotoxic T Cells ◽  
Cd4 T Cell ◽  
Chronic Inflammatory Diseases ◽  
The Common

Immunosenescence is thought to contribute to the increase of autoimmune diseases in older people. Immunosenescence is often associated with the presence of an expanded population of CD4 T cells lacking expression of CD28 (CD28null). These highly cytotoxic CD4 T cells were isolated from disease-affected tissues in patients with rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, or other chronic inflammatory diseases and their numbers appeared to be linked to disease severity. However, we recently demonstrated that the common herpes virus, cytomegalovirus (CMV), not ageing, is the major driver of this subset of cytotoxic T cells. In this review, we discuss how CMV might potentiate and exacerbate autoimmune disease through the expansion of CD28null CD4 T cells.

scholarly journals CD4 + T cells in inflammatory diseases : pathogenic T-helper cells and the CD69–Myl9 system

2021 ◽  
Author(s):  
Toshinori Nakayama ◽  
Kiyoshi Hirahara ◽  
Motoko Y Kimura ◽  
Chiaki Iwamura ◽  
Masahiro Kiuchi ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Inflammatory Diseases ◽  
Th2 Cells ◽  
T Helper ◽  
Activated T Cells ◽  
Th Cells ◽  
Inflammatory Lesions ◽  
Chronic Inflammatory Diseases ◽  
Disease Induction

Abstract CD4 + T cells direct immune responses against infectious microorganisms but are also involved in the pathogenesis of inflammatory diseases. In the last two to three decades, various researchers have identified and characterized several functional CD4 + T cell subsets, including T-helper 1 (Th1), Th2, Th9 and Th17 cells and regulatory T (Treg) cells. In this mini-review, we introduce the concept of pathogenic Th cells that induce inflammatory diseases with a model of disease induction by a population of pathogenic Th cells; “pathogenic Th population disease-induction model”. We will focus on Th2 cells that induce allergic airway inflammation—pathogenic Th2 cells (Tpath2 cells)—and discuss the nature of Tpath2 cells that shape the pathology of chronic inflammatory diseases. Various Tpath2 cell subsets have been identified and their unique features are summarized in mouse and human systems. Second, we will discuss how Th cells migrate and are maintained in chronic inflammatory lesions. We propose a model known as the “CD69–Myl9 system”. CD69 is a cell surface molecule expressed on activated T cells and interaction with its ligand myosin light chain 9 (Myl9) is required for the induction of inflammatory diseases. Myl9 molecules in the small vessels of inflamed lungs may play a crucial role in the migration of activated T cells into inflammatory lesions. Emerging evidence may provide new insight into the pathogenesis of chronic inflammatory diseases and contribute to the development of new therapeutic strategies for intractable inflammatory disorders.

scholarly journals CD44 and PSGL-1 Collaborate in Controlling the Migration of Human Activated T-Cells

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 3429-3429
Author(s):  
Amal J. Ali ◽  
Jasmeen S. Merzaban ◽  
Ayman F. Abuelela
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Conflicts Of Interest ◽  
Inflammatory Diseases ◽  
Activated T Cells ◽  
Selectin Ligands ◽  
Selectin Ligand ◽  
Mass Spectrometric Approach ◽  
First Time

Abstract Selectins play a central role in the trafficking of activated T cells by mediating tethering and rolling on vascular endothelium, acting as a beacon to help navigate them to the site of infection. Here we present a comprehensive binding and in vitro functional analysis of E-selectin ligands expressed on human activated T cells. Using a mass-spectrometric approach we identified a number of glycoproteins that may act as physiological E-selectin ligands on human activated T cells and focused on comparing the role the previously identified well-known E-selectin ligands, PSGL-1 (P-selectin glycoprotein ligand 1) to the newly identified ligand CD44. We show that CD44 from human activated CD4+ and CD8+ T cells binds E-selectin, and that immobilized CD44 mediates tethering and rolling of E-selectin expressing CHO cells via sialylated N-linked glycans. By knocking down CD44 and/or PSGL-1 in primary human activated T cells, our data demonstrate for the first time that CD44 is essential for mediating the rolling over E-selectin and thereby cooperates with PSGL-1 as a major E-selectin ligand on human activated T cells. This has major implications in the development of targeted therapies to combat inflammatory diseases and in transplantation settings. Disclosures No relevant conflicts of interest to declare.

scholarly journals Immune-enhancing effects of glucocorticoids in response to day–night cycles and stress

2020 ◽  
Vol 32 (11) ◽  
pp. 703-708 ◽  
Author(s):  
Akihiro Shimba ◽  
Koichi Ikuta
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Cd8 T Cells ◽  
Inflammatory Diseases ◽  
High Stress ◽  
Active Phase ◽  
Negative Effects ◽  
Memory Cd8 T Cells ◽  
Th17 Cell Differentiation ◽  
And Function

Abstract Environmental cues such as the day–night cycle or stressors trigger the production of glucocorticoids (GCs) by the adrenal cortex. GCs are well known for their anti-inflammatory effects that suppress the production of inflammatory cytokines and induce the apoptosis of lymphocytes. Recent studies in mice, however, have revealed pro-inflammatory effects. The diurnal oscillation of GCs induces the expression of IL-7 receptor α (IL-7Rα) and C–X–C motif chemokine receptor 4 (CXCR4) at the active phase, which drives the diurnal homing of T cells into lymphoid organs. This accumulation of T cells at the active phase enhances T-cell priming against bacterial infection and antigen immunization, leading to an increase of effector CD8 T cells and antibody production. GCs induced by moderate stress trigger the homing of memory CD8 T cells into the bone marrow and support the maintenance and response of these cells. Thus, endogenous GCs have a self-defense function to enhance adaptive immune responses. By contrast, strong stress induces even higher GC levels and causes chronic inflammation and autoimmunity. Because GCs can enhance the differentiation and function of T-helper 2 (Th2) and Th17 cells, high stress-induced GC levels might enhance inflammation via Th17 cell differentiation. Overall, the positive and negative effects of GCs may regulate the balance between normal immune responses and susceptibility to infections and inflammatory diseases.

scholarly journals Interleukin-21 in Viral Infections

2021 ◽  
Vol 22 (17) ◽  
pp. 9521
Author(s):  
Hironobu Asao
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Viral Infections ◽  
Inflammatory Diseases ◽  
Great Influence ◽  
Follicular Helper ◽  
Chronic Viral Infections ◽  
Microbial Infections ◽  
Autoimmune And Inflammatory Diseases ◽  
And Function

Interleukin (IL)-21 is a cytokine that affects the differentiation and function of lymphoid and myeloid cells and regulates both innate and adaptive immune responses. In addition to regulating the immune response to tumor and viral infections, IL-21 also has a profound effect on the development of autoimmune and inflammatory diseases. IL-21 is produced mainly from CD4+ T cells—in particular, follicular helper T (Tfh) cells—which have a great influence on the regulation of antibody production. It is also an important cytokine for the activation of CD8+ T cells, and its role in recovering the function of CD8+ T cells exhausted by chronic microbial infections and cancer has been clarified. Thus, IL-21 plays an extremely important role in viral infections, especially chronic viral infections. In this review, I will introduce the findings to date on how IL-21 is involved in some typical viral infections and the potential of treating viral diseases with IL-21.

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