scholarly journals The Immunoregulation of Th17 in Host against Intracellular Bacterial Infection

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Yonghong Li ◽  
Chaojun Wei ◽  
Hui Xu ◽  
Jing Jia ◽  
Zhenhong Wei ◽  
...  
Keyword(s):  
Protective Immunity ◽  
Bacterial Infections ◽  
Cytokine Production ◽  
T Helper ◽  
T Regulatory Cell ◽  
T Helper 17 ◽  
Socioeconomic Burden ◽  
Production Pattern ◽  
Underlying Mechanisms

T helper 17 cells (Th17) constitute a distinct subset of helper T cells with a unique transcriptional profile (STAT3, RORγ, and RORα), cytokine production pattern (IL17 family), and requirement of specific cytokines for their differentiation (TGF-β, IL6, IL21, and IL23). Recent studies involving experimental animals and humans have shown that Th17/IL17 plays a crucial role in host defense against a variety of pathogens, including bacteria and viruses. The underlying mechanisms by which Th17 performs include dendritic cell (DC) regulation, neutrophil recruitment, Th1 modulation, and T regulatory cell (Treg) balance. In recent years, researchers have generated an accumulating wealth of evidence on the role of Th17/IL17 in protective immunity to intracellular bacterial pathogens, such asMycobacterium tuberculosisandChlamydia trachomatis, which are one of the most important pathogens that inflict significant socioeconomic burden across the globe. In this article, we reviewed the current literature on the functions and mechanisms by which Th17/IL17 responds to intracellular bacterial infections. A better understanding of Th17/IL17 immunity to pathogens would be crucial for developing effective prophylactics and therapeutics.

scholarly journals Advances in T Helper 17 Cell Biology: Pathogenic Role and Potential Therapy in Multiple Sclerosis

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Elisabetta Volpe ◽  
Luca Battistini ◽  
Giovanna Borsellino
Keyword(s):  
Multiple Sclerosis ◽  
Cell Biology ◽  
Th17 Cells ◽  
Bacterial Infections ◽  
Demyelinating Diseases ◽  
T Helper ◽  
Pathogenic Role ◽  
T Helper 17 ◽  
Effector Cytokines

The discovery of the T helper (Th) 17 lineage, involved in the protection against fungal and extracellular bacterial infections, has profoundly revolutionized our current understanding of T cell-mediated responses in autoimmune diseases, including multiple sclerosis (MS). Indeed, recent data demonstrate the pathogenic role of Th17 cells in autoimmune disorders. In particular, studies in MS and in its animal model (EAE, experimental autoimmune encephalomyelitis) have revealed a crucial role of Th17 cells in the pathogenesis of autoimmune demyelinating diseases in both mice and humans. Over the past years, several important aspects concerning Th17 cells have been elucidated, such as the factors which promote or inhibit their differentiation and the effector cytokines which mediate their responses. The identification of the features endowing Th17 cells with high pathogenicity in MS is of particular interest, and discoveries in Th17 cell biology and function could lead to the design of new strategies aimed at modulating the immune response in MS. Here, we will discuss recent advances in this field, with particular focus on the mechanisms conferring pathogenicity in MS and their potential modulation.

scholarly journals The Alterations in and the Role of the Th17/Treg Balance in Metabolic Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Siwen Zhang ◽  
Xiaokun Gang ◽  
Shuo Yang ◽  
Mengzhao Cui ◽  
Lin Sun ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Metabolic Diseases ◽  
Treg Cells ◽  
Metabolic Dysfunction ◽  
T Helper ◽  
T Helper 17 ◽  
Glucose And Lipid Metabolism ◽  
Underlying Mechanisms

Chronic inflammation plays an important role in the development of metabolic diseases. These include obesity, type 2 diabetes mellitus, and metabolic dysfunction-associated fatty liver disease. The proinflammatory environment maintained by the innate immunity, including macrophages and related cytokines, can be influenced by adaptive immunity. The function of T helper 17 (Th17) and regulatory T (Treg) cells in this process has attracted attention. The Th17/Treg balance is regulated by inflammatory cytokines and various metabolic factors, including those associated with cellular energy metabolism. The possible underlying mechanisms include metabolism-related signaling pathways and epigenetic regulation. Several studies conducted on human and animal models have shown marked differences in and the important roles of Th17/Treg in chronic inflammation associated with obesity and metabolic diseases. Moreover, Th17/Treg seems to be a bridge linking the gut microbiota to host metabolic disorders. In this review, we have provided an overview of the alterations in and the functions of the Th17/Treg balance in metabolic diseases and its role in regulating immune response-related glucose and lipid metabolism.

scholarly journals Leptin promoted glycolytic metabolism to induce DCs activation via STAT3-HK2 pathway

2021 ◽  
Author(s):  
Yunshan Ye ◽  
Ziran Bai ◽  
Xiaokang Ye ◽  
Bo Yuan ◽  
Yawei Tang ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Mononuclear Cells ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Glycolytic Metabolism ◽  
T Helper ◽  
T Helper 17 ◽  
Peripheral Blood Mononuclear ◽  
Underlying Mechanisms

Leptin is over-secreted in many autoimmune diseases, which can promote dendritic cells (DCs) maturation and up-regulate the expression of inflammatory cytokines, but the underlying mechanisms are not fully elucidated. Considering the major role of leptin in maintaining energy balance and the significant role of glycolysis in DCs activation, our study aims to investigate whether leptin promotes the activation of DCs via glycolysis and its underlying mechanisms. We demonstrated that leptin promoted the activation of DCs, including up-regulating the expression of co-stimulatory molecules and inflammatory cytokines, enhancing the proliferation and T helper 17 (Th17) cell ratio in peripheral blood mononuclear cells (PBMC) co-cultured with leptin-stimulated DCs. Leptin also enhanced DCs glycolysis with increased glucose consumption, lactate production, and the expression of hexokinase 2 (HK2). In addition, the activation of DCs stimulated by leptin could be inhibited by the glycolysis inhibitor 2-DG. To explore the signaling pathways involved in leptin-induced HK2 expression, we observed that only the inhibitors of STAT3 (NSC74859) could repress the enhancement of HK2 triggered by leptin stimulation. Therefore, our results indicated that leptin promoted glycolytic metabolism to induce DCs activation via STAT3-HK2 pathway.

Assessment of the role of T Helper 17 cells in the pathogenesis of Acne Vulgaris

2019 ◽  
Vol 10 (12) ◽  
pp. 1435
Author(s):  
Nahla Maher ◽  
HebatAllah Ismail Gawdat ◽  
Heba Helmy El Hadidi ◽  
Olfat Gamil Shaker
Keyword(s):  
Acne Vulgaris ◽  
T Helper ◽  
T Helper 17 ◽  
T Helper 17 Cells

scholarly journals Placental ischemia-stimulated T-helper 17 cells induce preeclampsia-associated cytolytic natural killer cells during pregnancy

2018 ◽  
Vol 315 (2) ◽  
pp. R336-R343 ◽  
Author(s):  
Corbin A. Shields ◽  
Maggie McCalmon ◽  
Tarek Ibrahim ◽  
Dakota L. White ◽  
Jan M. Williams ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Natural Killer ◽  
Cell Activation ◽  
Fetal Weight ◽  
T Helper ◽  
T Helper 17 ◽  
Placental Ischemia ◽  
In Pregnancy

Previous studies have demonstrated that T-helper 17 (TH17) cells and cytolytic natural killer (cNK) cells are increased in women with preeclampsia. In this study we investigated the role of placental ischemia-stimulated TH17 cells in induction of cNK cells in pregnancy. We further assessed the role of TH17 cell-mediated oxidative stress in facilitation of cNK cell activation in pregnancy by treating rats with the SOD mimetic tempol. CD4+/CD25− cells were isolated from reduced uterine perfusion pressure (RUPP) rats and differentiated into TH17 cells in vitro. On day 12 of gestation ( GD12), 1 × 106 placental ischemia-stimulated TH17 cells were injected into normal pregnant (NP) rats (NP + RUPP TH17 rats), and a subset of rats were treated with tempol (30 mg·kg−1·day−1) from GD12 to GD19 (NP + RUPP TH17 + tempol rats). On GD19, cNK cells, mean arterial pressure, fetal weight, and cNK cell-associated cytokines and proteins were measured. Placental cNK cells were 2.9 ± 1, 14.9 ± 4, and 2.8 ± 1.0% gated in NP, NP + RUPP TH17, and NP + RUPP TH17 + tempol rats, respectively. Mean arterial pressure increased from 96 ± 5 mmHg in NP rats to 118 ± 2 mmHg in NP + RUPP TH17 rats and was 102 ± 3 mmHg in NP + RUPP TH17 + tempol rats. Fetal weight was 2.37 ± 0.04, 1.95 ± 0.14, and 2.3 ± 0.05 g in NP, NP + RUPP TH17, and NP + RUPP TH17 + tempol rats, respectively. Placental IFNγ increased from 1.1 ± 0.6 pg/mg in NP rats to 3.9 ± 0.6 pg/mg in NP + RUPP TH17 rats. Placental perforin increased from 0.18 ± 0.18 pg/mg in NP rats to 2.4 ± 0.6 pg/mg in NP + RUPP TH17 rats. Placental levels of granzymes A and B followed a similar pattern. Treatment with tempol did not lower placental cNK cytokines or proteins. The results of the present study identify TH17 cells as a mediator of aberrant NK cell activation that is associated with preeclampsia.

scholarly journals Pivotal Roles of T-Helper 17-Related Cytokines, IL-17, IL-22, and IL-23, in Inflammatory Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Ning Qu ◽  
Mingli Xu ◽  
Izuru Mizoguchi ◽  
Jun-ichi Furusawa ◽  
Kotaro Kaneko ◽  
...  
Keyword(s):  
Th17 Cell ◽  
Th17 Cells ◽  
Functional Role ◽  
Inflammatory Diseases ◽  
Interleukin 17 ◽  
T Helper ◽  
T Helper 17 ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

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.

scholarly journals 411 A new T helper 17 cytokine in hidradenitis suppurativa: antimicrobial and pro-inflammatory role of IL-26

2019 ◽  
Vol 139 (9) ◽  
pp. S285
Author(s):  
E. Scala ◽  
R. Di Caprio ◽  
S. Cacciapuoti ◽  
G. Caiazzo ◽  
A. Fusco ◽  
...  
Keyword(s):  
Hidradenitis Suppurativa ◽  
T Helper ◽  
T Helper 17

scholarly journals Interleukin-7 Produced by Intestinal Epithelial Cells in Response to Citrobacter rodentium Infection Plays a Major Role in Innate Immunity against This Pathogen

2015 ◽  
Vol 83 (8) ◽  
pp. 3213-3223 ◽  
Author(s):  
Wei Zhang ◽  
Jiang-Yuan Du ◽  
Qing Yu ◽  
Jun-O Jin
Keyword(s):  
Epithelial Cells ◽  
Protective Immunity ◽  
Bacterial Infections ◽  
Intestinal Epithelial Cells ◽  
Intestinal Damage ◽  
Intestinal Epithelial ◽  
Citrobacter Rodentium ◽  
Content Type ◽  
Interleukin 7

Interleukin-7 (IL-7) engages multiple mechanisms to overcome chronic viral infections, but the role of IL-7 in bacterial infections, especially enteric bacterial infections, remains unclear. Here we characterized the previously unexplored role of IL-7 in the innate immune response to the attaching and effacing bacteriumCitrobacter rodentium.C. rodentiuminfection induced IL-7 production from intestinal epithelial cells (IECs). IL-7 production from IECs in response toC. rodentiumwas dependent on gamma interferon (IFN-γ)-producing NK1.1+cells and IL-12. Treatment with anti-IL-7Rα antibody duringC. rodentiuminfection resulted in a higher bacterial burden, enhanced intestinal damage, and greater weight loss and mortality than observed with the control IgG treatment. IEC-produced IL-7 was only essential for protective immunity againstC. rodentiumduring the first 6 days after infection. An impaired bacterial clearance upon IL-7Rα blockade was associated with a significant decrease in macrophage accumulation and activation in the colon. Moreover,C. rodentium-induced expansion and activation of intestinal CD4+lymphoid tissue inducer (LTi) cells was completely abrogated by IL-7Rα blockade. Collectively, these data demonstrate that IL-7 is produced by IECs in response toC. rodentiuminfection and plays a critical role in the protective immunity against this intestinal attaching and effacing bacterium.

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