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T Cell Vaccination Inhibits Th1/Th17/Tfh Frequencies and Production of Autoantibodies in Collagen-Induced Arthritis  [PDF]
Shan Li,Xiaoyin Niu,Yebin Xi,Shaohua Deng,Chengzhen Li,Qing Zhao,Guangjie Chen
Journal of Immunology Research , 2013, DOI: 10.1155/2013/967301
Abstract: The aim of this study is to determine whether the regulatory role of T cell vaccination (TCV) is through inhibition of Th1/Th17/Tfh and production of autoantibodies on collagen-induced arthritis (CIA). First, CIA mice were treated with TCV. After disease onset, the incidence and severity of change in joint histopathology were evaluated. Mice in the TCV-treated group showed less disease severity and less infiltration of inflammatory cells in the joint sections. TCV decreased the frequencies of Th1/Th17/Tfh cells and related cytokines. Reduction of IL-21 may be associated with both Tfh and Th17, which further influence B cell and T cell responses. In addition, inhibition of Th1/Th17/Tfh frequencies led to the reduced expression of T-bet, RORα, RORγt, and Bcl6. Lastly, the proliferation of type-II-collagen-(CII-) specific T cells and the production of anti-CII antibodies were inhibited in the TCV-treated group. The results provide novel evidence that the therapeutic effects of TCV on CIA are associated with the inhibition of Th1/Th17/Tfh frequencies and autoantibodies production. 1. Introduction Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology, characterized by the presence of inflammatory synovitis accompanied by the destruction of joint cartilage and bone [1]. Collagen-induced arthritis (CIA) represents an animal model of autoimmune polyarthritis with significant similarities to human rheumatoid arthritis that can be induced upon immunization with native type II collagen. Both CIA and RA are characterized by manifestations of cellular as well as humoral autoimmunity, which may act in concert to mediate disease progression. T cell vaccination (TCV) has been reported to be effective in many autoimmune diseases, including experimental autoimmune encephalomyelitis and experimental arthritis [2–4]. TCV appears to induce regulatory immune responses through interactions of the host immune system with vaccine T cells, in both experimental animal models and humans [5]. It activates anti-idiotypic T cells by cytotoxic activity and antibody responses that react specifically with the T cell receptor (TCR) of vaccine T cells. It induces upregulation of Foxp3 expression and the inhibitory function of CD4+ CD25+ Tregs, which plays an important role in the regulation of autoreactive T cells and autoimmune diseases [6–9]. Recently, a body of evidence suggested that uncontrolled and persistent Th1, Th17 cells responses and their derived cytokines can contribute to autoimmune diseases, including RA [10]. Follicular helper T (Tfh) cells, a recently
Circulating Th22 and Th9 Levels in Patients with Acute Coronary Syndrome  [PDF]
Ying-zhong Lin,Bang-wei Wu,Zheng-de Lu,Ying Huang,Ying Shi,Hao Liu,Ling Liu,Qiu-tang Zeng,Xiang Wang,Qing-wei Ji
Mediators of Inflammation , 2013, DOI: 10.1155/2013/635672
Abstract: Background. CD4+ T helper (Th) cells play critical roles in the development and progression of atherosclerosis and the onset of acute coronary syndromes (ACS, including acute myocardial infarction (AMI) and unstable angina pectoris (UAP)). In addition to Th1, Th2, and Th17 cells, Th22 and Th9 subsets have been identified in humans. In the present study, we investigated whether Th22 cells and Th9 cells are involved in the onset of ACS. Methods. The frequencies of Th22 and Th9 cells were detected using a flow cytometric analysis and their related cytokine and transcription factor were measured in the AMI, UAP, stable angina pectoris (SAP), and control groups. Results. The results revealed a significant increase in the peripheral Th22 number, AHR expression, and IL-22 levels in patients with ACS compared with those in the SAP and control groups. Although there was no difference in the peripheral Th9 number among the four groups, the PU.1 expression and IL-9 levels were significantly increased in patients with ACS compared with the SAP and control groups. Conclusions. Circulating Th22 and Th9 type responses may play a potential role in the onset of ACS symptom. 1. Introduction CD4+ T helper (Th) cells play major roles in the inflammatory process of atherosclerosis and the onset of acute coronary syndromes (ACS) including unstable angina pectoris (UAP) and acute myocardial infarction (AMI) [1–3]. CD4+ Th cells, accompanied by macrophages and dendritic cells, are easily detected in the shoulders of plaque and lead to thrombosis, embolization, and varying degrees of obstruction of myocardial perfusion [4–6]. CD4+ Th cells include effector T cells, which protect against pathogens, and regulatory T cells (Tregs), which protect against effector responses to autoantigens and against responses to exogenous antigens that are harmful to the host. Based on their cytokine secretion profile, effector T cells are functionally subdivided into three types, Th1, Th2, and Th17. The roles of four CD4+ Th cell lineages, Th1, Th2, Th17, and Treg cells, in atherosclerosis are widely studied [1, 2]. During the past two decades, the Th1/Th2 paradigm prevailed, and Th1 cells were thought to promote the pathology in atherosclerosis and Th2 cells were thought to attenuate the disease [7–9]. Recently, Th17, the third subpopulation of Th cells, was found to promote atherosclerotic lesion development in atherosclerotic-prone models and it was related to the onset of coronary artery disease in a number of studies [10–12]. The role of Th17 in atherosclerosis remains uncertain. Although
Increased Frequencies of Th22 Cells as well as Th17 Cells in the Peripheral Blood of Patients with Ankylosing Spondylitis and Rheumatoid Arthritis  [PDF]
Lei Zhang, Yong-gang Li, Yu-hua Li, Lei Qi, Xin-guang Liu, Cun-zhong Yuan, Nai-wen Hu, Dao-xin Ma, Zhen-feng Li, Qiang Yang, Wei Li, Jian-min Li
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0031000
Abstract: Background T-helper (Th) 22 is involved in the pathogenesis of inflammatory diseases. The roles of Th22 cells in the pathophysiological of ankylosing spondylitis (AS) and rheumatoid arthritis (RA) remain unsettled. So we examined the frequencies of Th22 cells, Th17 cells and Th1 cells in peripheral blood (PB) from patients with AS and patients with RA compared with both healthy controls as well as patients with osteoarthritis. Design and Methods We studied 32 AS patients, 20 RA patients, 10 OA patients and 20 healthy controls. The expression of IL-22, IL-17 and IFN-γ were examined in AS, RA, OA patients and healthy controls by flow cytometry. Plasma IL-22 and IL-17 levels were examined by enzyme-linked immunosorbent assay. Results Th22 cells, Th17 cells and interleukin-22 were significantly elevated in AS and RA patients compared with OA patients and healthy controls. Moreover, Th22 cells showed positive correlation with Th17 cells as well as interleukin-22 in AS and RA patients. However, positive correlation between IL-22 and Th17 cells was only found in AS patients not in RA patients. In addition, the percentages of both Th22 cells and Th17 cells correlated positively with disease activity only in RA patients not in AS patients. Conclusions The frequencies of both Th22 cells and Th17 cells were elevated in PB from patients with AS and patients with RA. These findings suggest that Th22 cells and Th17 cells may be implicated in the pathogenesis of AS and RA, and Th22 cells and Th17 cells may be reasonable cellular targets for therapeutic intervention.
Elevated Peripheral Frequencies of Th22 Cells: A Novel Potent Participant in Obesity and Type 2 Diabetes  [PDF]
Ruxing Zhao, Dongqi Tang, Shounan Yi, Wenjuan Li, Chuanlong Wu, Yiran Lu, Xinguo Hou, Jun Song, Peng Lin, Li Chen, Lei Sun
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0085770
Abstract: Objective Chronic low-grade inflammation has long been recognized as the central link between obesity and type 2 diabetes (T2D). The novel subset of T helper (Th) cells, Th22, plays an emerging role in chronic inflammation. We investigated the potential association between Th22 and the pathogenesis of obesity and T2D. Methods Ninety T2D inpatients (T2D group), 30 healthy participants with BMI ranged from 19 to 23.9 kg/m2 (CTL group) and 30 metabolically healthy obese controls with BMI ≥ 30 kg/m2 (MHO group) were employed in our study. Peripheral frequencies of Th22 and Th1 and Th17 cells were determined by flow cytometry based on their specific cytokine patterns. Cytokine levels in fresh plasma were quantified by ELISA. Results Compared to that in CTL group (1.18±0.06%, n = 28), peripheral frequency of Th22 cells was significantly increased in MHO group (1.88±0.10%, n = 30) and in T2D group (2.247±0.10%, n = 89). There was a consistent notable increase in plasma interleukin (IL)-22 of T2D patients [47.56 (30.55–76.89) pg/mL] as compared with that of MHO group [36.65 (29.52–55.70) pg/ml; *P<0.0001] and CTLs [36.33 (31.93–40.62) pg/mL; *P<0.0001]. Furthermore, other than Th1/Th17, previously frequently described participants in obesity and T2D, there was a strong correlation between Th22 frequency and the homeostasis model of assessment for insulin resistance index (r = 0.6771, *P<0.0001) and HOMA for β-cell function (r = ?0.7264, *P<0.0001). Conclusions There were increased Th22 frequencies and IL-22 levels in obesity and T2D. Elevated Th22 and IL-22 also aided in the differentiation of MHO from T2D patients. The notable correlation implied that Th22 might play a more determinant role in both insulin resistance and β-cell impairment.
Serum Levels of Selected Th17 and Th22 Cytokines in Psoriatic Patients  [PDF]
Anna Michalak-Stoma,Joanna Bartosińska,Ma?gorzata Kowal,Maria Juszkiewicz-Borowiec,Agnieszka Gerkowicz,Gra?yna Chodorowska
Disease Markers , 2013, DOI: 10.1155/2013/856056
Abstract: Introduction. Psoriasis is a T cell-mediated inflammatory disease in which pathogenesis T helper (Th) lymphocytes (Th1, Th17, and Th22) play an important role. The aim of the study was to assess the serum levels of some cytokines involved in the Th17 and Th22 responses in psoriatic patients. Material and Methods. The study comprised 60 psoriatic patients and 30 healthy controls. In the serum collected from psoriatic patients and healthy controls, the concentrations of IL-6, IL-12, IL-17, IL-20, IL-22, and IL-23 were examined with ELISA kits. Severity of psoriatic skin lesions was assessed by means of PASI, BSA, and PGA scores. Results. IL-6, IL-20, and IL-22 concentrations were significantly higher in psoriatic patients in comparison with the control group. The positive correlations between the concentrations of IL-22 and IL-20 and severity of psoriasis assessed with PASI and BSA scores as well as IL-17 and PASI score were found. There was also a positive correlation between IL-23 and IL-17 concentrations. Conclusions. Results of the conducted studies suggest that Th22 response may contribute to the skin and systemic inflammatory disease in psoriasis. It seems that early identification of soluble biomarkers and initiation of well-matched treatment may prevent exacerbation and progression of psoriasis. 1. Introduction The knowledge about the role of cytokines in psoriasis has developed in the last several years. Initially, only Th1 cells and cytokines secreted by these cells, like TNF-α, IFN-γ, and IL-2, have been associated with the development and maintenance of chronic inflammatory diseases, such as psoriasis. Th1 cells differentiate from naive CD4+ cells in the presence of IL-12, IL-18, and IFNα and γ. It is well known that Th1 cytokines have strong inflammatory effects in activating macrophage, neutrophil, and CD8+ cytotoxic T cells [1]. In the 1990s, Th17 cells were described as a new T-cell population that produces IL-17, IL-6, IL-21, IL-22, and TNF [2]. Transforming growth factor (TGF)-β1, IL-6, IL-23, and IL-15 stimulated initial Th17 differentiation from naive T cells [3]. TGF-β1 is secreted by activated T cells and it initiates T cell and fibroblast activation, as well as angiogenesis and neovascularization [3–7]. IL-6, secreted by macrophages, endothelial cells, and epithelial cells, is responsible for augmentation of keratinocyte hyperplasia and invasion of macrophages and T cells [3, 8]. IL-15, produced by monocytes, macrophages, DCs, and T cells, can appear to induce angiogenesis, immune cell recruitment, and activation of keratinocytes
TH17, TH22 and TReg Cells Are Enriched in the Healthy Human Cecum  [PDF]
Martin J. Wolff, Jacqueline M. Leung, Michael Davenport, Michael A. Poles, Ilseung Cho, P'ng Loke
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041373
Abstract: There is increasing evidence that dysregulation of CD4+ T cell populations leads to intestinal inflammation, but the regional distribution of these populations throughout the intestinal tract in healthy individuals remains unclear. Here, we show that TH17, TH22 and TReg cells are enriched in the healthy human cecum compared to the terminal ileum and sigmoid colon, whereas TH1 and TH2 cells do not significantly vary by location. Transcriptional profiling analysis of paired pinch biopsies from different regions of the intestine identified significant differences in the metabolic state of the terminal ileum, cecum, and sigmoid colon. An increased proportion of TH17 cells was positively associated with expression of resistin (RETN) and negatively associated with expression of trefoil factor 1 (TFF1). These results suggest that CD4+ T helper cells that are important in maintaining mucosal barrier function may be enriched in the cecum as a result of metabolic differences of the surrounding microenvironment.
Increased frequency of circulating Th22 in addition to Th17 and Th2 lymphocytes in systemic sclerosis: association with interstitial lung disease
Marie-Elise Truchetet, Nicolò C Brembilla, Elisa Montanari, Yannick Allanore, Carlo Chizzolini
Arthritis Research & Therapy , 2011, DOI: 10.1186/ar3486
Abstract: Clinical data and peripheral blood were collected in 33 SSc individuals and 29 HD. IL-17A, IL-22, interferon gamma (IFN-γ), IL-4 production, the chemokine receptors CCR4, CCR6, CCR10, CXCR3 expression and the CD161 Th17 cell marker were assessed by multiparametric flow cytometry in PB CD4+ T cells. Intracellular cytokine accumulation was further investigated in CD4+ T cells expanded in vitro for seven days.The frequency of Th22, Th17, Th2, but not Th1 cells, was significantly increased in SSc individuals compared to HD. The percentage of CD161+CD4+ T cells was increased in SSc and correlated with the percentage of IL-17A producing cells. Moreover, the expression of the skin- and lung-homing chemokine receptor CCR6 correlated with the frequency of IL-22 and IL-17A-producing cells in SSc but not in HD. Finally, SSc interstitial lung disease (ILD) was strongly associated with higher numbers of IL-22 and, to a lesser extent, IL-17A-producing cells.IL-22 and IL-17A-producing T cells with skin- and lung-homing capabilities are characteristically increased in SSc. These findings support the hypothesis that Th22, in addition to Th17 cells, may be involved in pathological processes leading to SSc. While the association between IL-22 producing cells and ILD needs to be assessed in larger cohorts of patients, the increased frequency of Th22 cells appears to be a useful novel biomarker in SSc.Systemic sclerosis (SSc), or scleroderma, is a chronic connective tissue disease characterized by autoimmunity, fibrosis of the skin and internal organs, and vascular dysfunction [1]. While the pathogenic mechanisms of the disease are still largely elusive, a number of findings indicate that the immune response may play a key role [2]. First, antinuclear antibodies (ANA) are characteristically present and segregate with distinct clinical presentations. Second, genetic studies indicate that most of the gene polymorphisms associated with SSc involve genes coding for molecules controlling the
Dendritic Cell-Induced Th1 and Th17 Cell Differentiation for Cancer Therapy  [PDF]
Julia Terhune,Erik Berk,Brian J. Czerniecki
Vaccines , 2013, DOI: 10.3390/vaccines1040527
Abstract: The success of cellular immunotherapies against cancer requires the generation of activated CD4 + and CD8 + T-cells. The type of T-cell response generated (e.g., Th1 or Th2) will determine the efficacy of the therapy, and it is generally assumed that a type-1 response is needed for optimal cancer treatment. IL-17 producing T-cells (Th17/Tc17) play an important role in autoimmune diseases, but their function in cancer is more controversial. While some studies have shown a pro-cancerous role for IL-17, other studies have shown an anti-tumor function. The induction of polarized T-cell responses can be regulated by dendritic cells (DCs). DCs are key regulators of the immune system with the ability to affect both innate and adaptive immune responses. These properties have led many researchers to study the use of ex vivo manipulated DCs for the treatment of various diseases, such as cancer and autoimmune diseases. While Th1/Tc1 cells are traditionally used for their potent anti-tumor responses, mounting evidence suggests Th17/Tc17 cells should be utilized by themselves or for the induction of optimal Th1 responses. It is therefore important to understand the factors involved in the induction of both type-1 and type-17 T-cell responses by DCs.
T Helper Cell Subsets Specific for Pseudomonas aeruginosa in Healthy Individuals and Patients with Cystic Fibrosis  [PDF]
Hannah K. Bayes, Stephen Bicknell, Gordon MacGregor, Tom J. Evans
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0090263
Abstract: Background We set out to determine the magnitude of antigen-specific memory T helper cell responses to Pseudomonas aeruginosa in healthy humans and patients with cystic fibrosis. Methods Peripheral blood human memory CD4+ T cells were co-cultured with dendritic cells that had been infected with different strains of Pseudomonas aeruginosa. The T helper response was determined by measuring proliferation, immunoassay of cytokine output, and immunostaining of intracellular cytokines. Results Healthy individuals and patients with cystic fibrosis had robust antigen-specific memory CD4+ T cell responses to Pseudomonas aeruginosa that not only contained a Th1 and Th17 component but also Th22 cells. In contrast to previous descriptions of human Th22 cells, these Pseudomonal-specific Th22 cells lacked the skin homing markers CCR4 or CCR10, although were CCR6+. Healthy individuals and patients with cystic fibrosis had similar levels of Th22 cells, but the patient group had significantly fewer Th17 cells in peripheral blood. Conclusions Th22 cells specific to Pseudomonas aeruginosa are induced in both healthy individuals and patients with cystic fibrosis. Along with Th17 cells, they may play an important role in the pulmonary response to this microbe in patients with cystic fibrosis and other conditions.
A High Frequency of Circulating Th22 and Th17 Cells in Patients with New Onset Graves’ Disease  [PDF]
Di Peng, Bingchuan Xu, Ye Wang, Hui Guo, Yanfang Jiang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0068446
Abstract: T-helper (Th) 22 and Th17 cells are involved in the pathogenesis of autoimmune diseases. However, their roles in the pathogenesis of Graves’disease (GD) are unclear. This study is aimed at examining the frequency of peripheral blood Th22, Th17, and Th1 cells and the levels of plasma IL-22, IL-17, and IFN-γ in patients with GD. A total of 27 patients with new onset GD and 27 gender- and age-matched healthy controls (HC) were examined for the frequency of peripheral blood Th22, Th17, and IFN-γ cells by flow cytometry. The concentrations of plasma IL-22, IL-17, and IFN-γ were examined by enzyme-linked immunosorbent assay. The levels of serum TSHR antibodies (A-TSHR), free triiodothyronine (FT3), free thyroxine (FT4), and thyroid stimulating hormone (TSH) were examined by radioimmunoassay and chemiluminescent assay, respectively. The levels of serum TSAb were examined by enzyme-linked immunosorbent assay. In comparison with those in the HC, significantly elevated percentages of Th22 and Th17 cells, but not Th1 cells, and increased levels of plasma IL-22 and IL-17, but not IFN-γ, were detected in GD patients (P<0.0001, for both). The percentages of both Th22 and Th17 cells and the levels of plasma IL-22 and IL-17 were correlated positively with the levels of serum TSAb in GD patients (r = 0.7944, P<0.0001; r = 0.8110, P<0.0001; r = 0.7101, p<0.0001; r = 0.7407, p<0.0001, respectively). Th22 and Th17 cells may contribute to the pathogenesis of GD.
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