Role of T Helper Lymphocytes in Autoimmune Diseases

1989 ◽  
pp. 117-131
Author(s):  
Gérald J. Prud’homme ◽  
Nollaig A. Parfrey
2013 ◽  
Vol 168 (1) ◽  
pp. R13-R18 ◽  
Author(s):  
Géraldine Falgarone ◽  
Hassan M Heshmati ◽  
Régis Cohen ◽  
Gérard Reach

The role of stress in the pathophysiology of Graves' disease is suggested by several clinical observations, by recent advances in immunology and by better understanding of autoimmune diseases which provides new insights into potential effects of stress hormones on T helper cell imbalance involved in the pathogenesis of autoimmune diseases. Stress management should therefore be an important part of the treatment of Graves' disease, as stress reduction may improve the effect of therapy. However, this field still requires interventional data to support stress management in the treatment of Graves' disease.


2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Aristo Vojdani ◽  
Jama Lambert

CD4+effector cells, based on cytokine production, nuclear receptors and signaling pathways, have been categorized into four subsets. T-helper-1 cells produce IFN-γ, TNF-β, lymphotoxin and IL-10; T-helper-2 cells produce IL-4, IL-5, IL-10, IL-13, IL-21 and IL-31; T-helper-3, or regulatory T-cells, produce IL-10, TGF-βand IL-35; and the recently discovered T-helper-17 cell produces IL-17, IL-17A, IL-17F, IL-21, IL-26 and CCL20. By producing IL-17 and other signaling molecules, Th17 contributes to the pathogenesis of multiple autoimmune diseases including allergic inflammation, rheumatoid arthritis, autoimmune gastritis, inflammatory bowel disease, psoriasis and multiple sclerosis. In this article, we review the differential regulation of inflammation in different tissues with a major emphasis on enhancement of neuroinflammation by local production of IL-17 in the brain. By understanding the role of pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting Th17 and associated cytokine activities and signaling pathways to repair the intestinal and blood-brain barriers for their patients with autoimmunities, in particular, those with neuroinflammation and neurodegeneration.


1993 ◽  
Vol 6 (5) ◽  
pp. 571-585 ◽  
Author(s):  
John Reynolds ◽  
Beverley A. Sallie ◽  
Christos Syrganis ◽  
Charles D. Pusey

2015 ◽  
Vol 7 (2) ◽  
pp. 62-67
Author(s):  
ASM Giasuddin ◽  
KA Jhuma ◽  
AMM Haq ◽  
MM Haque

Rheumatoid arthritis (RA) is a chronic inflammatory disease occurring three times more in females throughout the world affecting 1-2% of the adult population in all ethnic groups, usually in the age group of 25-60 years. Although the role of CD4 + T helper lymphocytes in the aetiopathogenesis has been studied for more than three decades, the focus on CD4 + T helper type 17 (Th17) lymphocytes and its associated cytokines is much more recent. The cytokines such as IL-17 and IFN-g induce secondary cytokines such as IL-1, TNF-a , etc which possibly cause inflammation in joints. This cytokine cascade, therefore, offers a number of points and opportunities for immunointervention in RA. The present review article highlights some of the major aspects of the immunopathogenesis that involve Th17 cells and their association relevant to recent developments in the treatment of RA. DOI: http://dx.doi.org/10.3329/bjmb.v7i2.22415 Bangladesh J Med Biochem 2014; 7(2): 62-67


2022 ◽  
Vol 12 ◽  
Author(s):  
Aurelie S. Clottu ◽  
Morgane Humbel ◽  
Natalia Fluder ◽  
Maria P. Karampetsou ◽  
Denis Comte

Innate lymphoid cells (ILC) are a heterogeneous group of immune cells characterized by lymphoid morphology and cytokine profile similar to T cells but which do not express clonally distributed diverse antigen receptors. These particular cells express transcription factors and cytokines reflecting their similarities to T helper (Th)1, Th2, and Th17 cells and are therefore referred to as ILC1, ILC2, and ILC3. Other members of the ILC subsets include lymphoid tissue inducer (LTi) and regulatory ILC (ILCreg). Natural killer (NK) cells share a common progenitor with ILC and also exhibit a lymphoid phenotype without antigen specificity. ILC are found in low numbers in peripheral blood but are much more abundant at barrier sites such as the skin, liver, airways, lymph nodes, and the gastrointestinal tract. They play an important role in innate immunity due to their capacity to respond rapidly to pathogens through the production of cytokines. Recent evidence has shown that ILC also play a key role in autoimmunity, as alterations in their number or function have been identified in systemic lupus erythematosus, systemic sclerosis, and rheumatoid arthritis. Here, we review recent advances in the understanding of the role of ILC in the pathogenesis of autoimmune diseases, with particular emphasis on their role as a potential diagnostic biomarker and as therapeutic targets.


Author(s):  
Rita GOLBAN

The scientific investigations reflected in this study present the research in dynamics of the activity of correlating T-helper and T-suppressor immunocompetent cells at the newborn calves in different age periods. In the scientific research is presented the main effector role of these indicators, regarding the importance of the immune system through the ability to synthesize lymphokines, etc. The researches reveal T-helper and T-suppressor level of lymphocytes at all research ages. Thus at 10 days the concentration of T-helper lymphocytes was 7.85±0.001 and 8.30±0.08; 7.57 ± 0.008 at the age of 20 and 30 days, compared to T-suppressor lymphocytes, which in these age groups was equal to 6.0 ± 0.08; 6.33 ± 0.08 and 6.0±0.08. The results of the investigations offer the possibility to understand that the correlation of some lymphocytary subpopulations of the newborn animal organism provides the possibility of installing a strong immunity and ensures the maintenance of the biochemical homeostasis of the organism.


2021 ◽  
Vol 7 (2) ◽  
pp. 137
Author(s):  
Eva Burger

Protective immunity against Paracoccidioides consists of a stepwise activation of numerous effector mechanisms that comprise many cellular and soluble components. At the initial phase of non-specific innate immunity, resistance against Paracoccidioides comes from phagocytic polymorphonuclear neutrophils, natural killer (NK) cells and monocytes, supplemented by soluble factors such as cytokines and complement system components. Invariant receptors (Toll-like receptors (TLRs), Dectins) which are present in cells of the immune system, detect patterns present in Paracoccidioides (but not in the host) informing the hosts cells that there is an infection in progress, and that the acquired immunity must be activated. The role of components involved in the innate immunity of paracoccidioidomycosis is herein presented. Humoral immunity, represented by specific antibodies which control the fungi in the blood and body fluids, and its role in paracoccidioidomycosis (which was previously considered controversial) is also discussed. The protective mechanisms (involving various components) of cellular immunity are also discussed, covering topics such as: lysis by activated macrophages and cytotoxic T lymphocytes, the participation of lytic products, and the role of cytokines secreted by T helper lymphocytes in increasing the efficiency of Paracoccidioides, lysis.


2019 ◽  
Author(s):  
Lindsay M. Webb ◽  
Shouvonik Sengupta ◽  
Claudia Edell ◽  
Stephanie A. Amici ◽  
Janiret Narvaez-Miranda ◽  
...  

AbstractProtein Arginine Methyltransferase (PRMT) 5 catalyzes symmetric dimethylation of arginine, a post-translational modification involved in cancer and embryonic development. However, the role of PRMT5 in T helper (Th) cell polarization and Th cell-mediated disease has not yet been elucidated. Here we report that PRMT5 is necessary for Th17 differentiation and EAE, via enhancement of cholesterol biosynthesis and activation of ROR-γt. PRMT5 additionally controls thymic and peripheral homeostasis in the CD4 Th cell life cycle, as well as iNK T and CD8 T cell development or maintenance, respectively. Overall, our two conditional PRMT5 KO models that selectively delete PRMT5 in all T cells (T-PRMT5Δ/Δ) or Th cells (iCD4-PRMT5Δ/Δ) unveil a crucial role for PRMT5 in T cell proliferation, Th17 responses and disease. These results point to Th PRMT5 and its downstream cholesterol biosynthesis pathway as promising therapeutic targets in Th17-mediated diseases.


2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Patricia Castro-Sánchez ◽  
Rocio Ramirez-Munoz ◽  
Pedro Roda-Navarro

Phosphotyrosine phosphatases (PTPs) constitute a complex family of enzymes that control the balance of intracellular phosphorylation levels to allow cell responses while avoiding the development of diseases. Despite the relevance of CD4 T cell polarisation and effector function in human autoimmune diseases, the expression profile of PTPs during T helper polarisation and restimulation at inflammatory sites has not been assessed. Here, a systematic analysis of the expression profile of PTPs has been carried out during Th1-polarising conditions and upon PKC activation and intracellular raise of Ca2+in effector cells. Changes in gene expression levels suggest a previously nonnoted regulatory role of several PTPs in Th1 polarisation and effector function. A substantial change in the spatial compartmentalisation of ERK during T cell responses is proposed based on changes in the dose of cytoplasmic and nuclear MAPK phosphatases. Our study also suggests a regulatory role of autoimmune-related PTPs in controlling T helper polarisation in humans. We expect that those PTPs that regulate T helper polarisation will constitute potential targets for intervening CD4 T cell immune responses in order to generate new therapies for the treatment of autoimmune diseases.


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