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 Targeting interleukin-17 in chronic inflammatory disease: A clinical perspective

2019 ◽  
Vol 217 (1) ◽  
Author(s):  
Pascale Zwicky ◽  
Susanne Unger ◽  
Burkhard Becher
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Diseases ◽  
Chronic Inflammatory Disease ◽  
Interleukin 17 ◽  
Clinical Perspective ◽  
Preclinical Models ◽  
Chronic Inflammatory Diseases ◽  
Recent Developments ◽  
Disease Entities ◽  
Barrier Tissues

Chronic inflammatory diseases like psoriasis, Crohn’s disease (CD), multiple sclerosis (MS), rheumatoid arthritis (RA), and others are increasingly recognized as disease entities, where dysregulated cytokines contribute substantially to tissue-specific inflammation. A dysregulation in the IL-23/IL-17 axis can lead to inflammation of barrier tissues, whereas its role in internal organ inflammation remains less clear. Here we discuss the most recent developments in targeting IL-17 for the treatment of chronic inflammation in preclinical models and in patients afflicted with chronic inflammatory diseases.

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 Superantigenic Staphylococcus aureus Stimulates Production of Interleukin-17 from Memory but Not Naive T Cells

2009 ◽  
Vol 78 (1) ◽  
pp. 381-386 ◽  
Author(s):  
Ulrika Islander ◽  
Annica Andersson ◽  
Erika Lindberg ◽  
Ingegerd Adlerberth ◽  
Agnes E. Wold ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Th17 Cells ◽  
Mononuclear Cells ◽  
Memory T Cells ◽  
Inflammatory Diseases ◽  
Commensal Bacteria ◽  
Interleukin 17 ◽  
T Helper ◽  
T Helper 17

ABSTRACT T-helper 17 (Th17) cells are characterized by their production of interleukin-17 (IL-17) and have a role in the protection against infections and in certain inflammatory diseases. Humans who lack Th17 cells are more susceptible to Staphylococcus aureus infections compared to individuals having Th17 cells. S. aureus is part of the commensal skin microflora and also colonize the infant gut. To investigate whether UV-killed S. aureus would be more capable of inducing IL-17 than other commensal bacteria, we stimulated mononuclear cells from adults, infants, and newborns with various gram-positive and gram-negative commensal bacteria. IL-17 was produced from adult memory Th17 cells after stimulation with superantigen-producing S. aureus but not nonsuperantigenic S. aureus or other common commensal gut bacteria. Cells from newborns were poor IL-17 producers after stimulation with S. aureus, whereas in some cases IL-17 was secreted from cells isolated from infants at the age of 4 and 18 months. These results suggest that superantigenic S. aureus are particularly efficient in stimulating IL-17 production and that the cytokine is produced from memory T cells.

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.

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 MAIT Cells Come to the Rescue in Cancer Immunotherapy?

Cancers ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 413 ◽  
Author(s):  
Zuzanna Lukasik ◽  
Dirk Elewaut ◽  
Koen Venken
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cancer Immunotherapy ◽  
Cell Biology ◽  
Inflammatory Diseases ◽  
Cell Subset ◽  
Adaptive Immune System ◽  
Mesenteric Lymph Nodes ◽  
Mait Cells ◽  
Invariant T Cells

Recent progress in immunobiology has led to the observation that, among cells classically categorized as the typical representatives of the adaptive immune system, i.e., T cells, some possess the phenotype of innate cells. Invariant T cells are characterized by T cell receptors recognizing a limited range of non-peptide antigens, presented only in the context of particular molecules. Mucosal-associated invariant T cells (MAIT cells) are an example of such unconventional cells. In humans, they constitute between 1% and 8% of the peripheral blood T lymphocytes and are further enriched in mucosal tissues, mesenteric lymph nodes, and liver, where they can account for even 40% of all the T cells. MAIT cells recognize antigens in the context of major histocompatibility complex class I-related protein (MR1). Upon activation, they instantly release pro-inflammatory cytokines and mediate cytolytic function towards bacterially infected cells. As such, they have been a rapidly evolving research topic not only in the field of infectious diseases but also in the context of many chronic inflammatory diseases and, more recently, in immuno-oncology. Novel findings suggest that MAIT cells function could also be modulated by endogenous ligands and drugs, making them an attractive target for therapeutic approaches. In this review, we summarize the current understanding of MAIT cell biology, their role in health and disease and discuss their future potential in cancer immunotherapy. This is discussed through the prism of knowledge and experiences with invariant natural killer T cells (iNKT)—another prominent unconventional T cell subset that shares many features with MAIT cells.

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