The Role of T-helper Lymphocytes in Priming for Experimental Autoimmune Glomerulonephritis in the BN Rat

1993 ◽  
Vol 6 (5) ◽  
pp. 571-585 ◽  
Author(s):  
John Reynolds ◽  
Beverley A. Sallie ◽  
Christos Syrganis ◽  
Charles D. Pusey
2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Ning Qu ◽  
Mingli Xu ◽  
Izuru Mizoguchi ◽  
Jun-ichi Furusawa ◽  
Kotaro Kaneko ◽  
...  

T-helper 17 (Th17) cells are characterized by producing interleukin-17 (IL-17, also called IL-17A), IL-17F, IL-21, and IL-22 and potentially TNF-α and IL-6 upon certain stimulation. IL-23, which promotes Th17 cell development, as well as IL-17 and IL-22 produced by the Th17 cells plays essential roles in various inflammatory diseases, such as experimental autoimmune encephalomyelitis, rheumatoid arthritis, colitis, and Concanavalin A-induced hepatitis. In this review, we summarize the characteristics of the functional role of Th17 cells, with particular focus on the Th17 cell-related cytokines such as IL-17, IL-22, and IL-23, in mouse models and human inflammatory diseases.


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


Endocrinology ◽  
2005 ◽  
Vol 146 (11) ◽  
pp. 4721-4726 ◽  
Author(s):  
Su He Wang ◽  
Zhengyi Cao ◽  
Julie M. Wolf ◽  
Mary Van Antwerp ◽  
James R. Baker

The role of TNF-related apoptosis-inducing ligand (TRAIL) in autoimmune thyroiditis is unclear. We used experimental autoimmune thyroiditis to clarify the contribution of TRAIL to the development of autoimmune thyroiditis. CBA/J mice were immunized with murine thyroglobulin, and spleen cells from these mice were subsequently injected into irradiated recipient CBA/J mice. One week later, the recipient mice were treated with recombinant TRAIL or a control protein. Compared with control animals, TRAIL-treated mice developed a milder form of the disease with a significant decrease in mononuclear cell infiltration in the thyroid and less thyroid follicular destruction. Furthermore, the number of apoptotic thyrocytes and also thyroglobulin-specific T helper-1 cell responses in TRAIL-treated mice was lower than that in the control animals. This study suggests that exogenous TRAIL suppresses the development of autoimmune thyroiditis via altering the function of cells involved in the immune response. These findings may contribute toward a novel treatment autoimmune thyroiditis.


1989 ◽  
pp. 117-131
Author(s):  
Gérald J. Prud’homme ◽  
Nollaig A. Parfrey

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.


Author(s):  
James Quinn ◽  
Robert Axtell

Multiple sclerosis is an autoimmune disorder where both T cells and B cells are implicated in pathology. However, it remains unclear how these two distinct populations cooperate to drive disease. There is ample evidence from studies in both MS patients and mouse models that Th17, B cells, and follicular T helper (TFH) cells contribute to disease. This review article describes the literature that identifies mechanisms by which Th17, TFH, and B cells cooperatively drive disease activity in MS and EAE. The curation of this literature has identified that CNS-infiltrating TFH cells act with TH17 cell to contribute to an inflammatory B cell response in neuroinflammation. This demonstrates that TFH cells and their products are promising targets for therapies in MS.


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.


2021 ◽  
Vol 22 (6) ◽  
pp. 2924
Author(s):  
Zahra Maria ◽  
Emma Turner ◽  
Agnieshka Agasing ◽  
Gaurav Kumar ◽  
Robert C. Axtell

Pertussis toxin (PTX) is a required co-adjuvant for experimental autoimmune encephalomyelitis (EAE) induced by immunization with myelin antigen. However, PTX’s effects on EAE induced by the transfer of myelin-specific T helper cells is not known. Therefore, we investigated how PTX affects the Th17 transfer EAE model (Th17-EAE). We found that PTX significantly reduced Th17-EAE by inhibiting chemokine-receptor-dependent trafficking of Th17 cells. Strikingly, PTX also promoted the accumulation of B cells in the CNS, suggesting that PTX alters the disease toward a B-cell-dependent pathology. To determine the role of B cells, we compared the effects of PTX on Th17-EAE in wild-type (WT) and B-cell-deficient (µMT) mice. Without PTX treatment, disease severity was equivalent between WT and µMT mice. In contrast, with PTX treatment, the µMT mice had significantly less disease and a reduction in pathogenic Th17 cells in the CNS compared to the WT mice. In conclusion, this study shows that PTX inhibits the migration of pathogenic Th17 cells, while promoting the accumulation of pathogenic B cells in the CNS during Th17-EAE. These data provide useful methodological information for adoptive-transfer Th17-EAE and, furthermore, describe another important experimental system to study the pathogenic mechanisms of B cells in multiple sclerosis.


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