Cell Subsets In Patients Research Articles

An Adaptive Control Scheme for Interleukin-2 Therapy.

SummaryRegulatory T cells (Treg) are suppressor cells that control self-reactive and excessive effector conventional T helper cell (Tconv) responses. Breakdown of the balance between Tregs and Tconvs is a hallmark of autoimmune and inflammatory diseases. Interleukin-2 (IL-2) is a growth factor for both populations and subtle leverage to restore the healthy immune balance in IL-2 therapy. By using a mechanistic mathematical model, we introduced an adaptive control strategy to design the minimal therapeutic IL-2 dosage required to increase and stabilize Treg population and restrict inflammatory response. This adaptive protocol allows for dose adjustments based on the feedback of the immune kinetics of the patient. Our simulation results showed that a minimal Treg population was required to restrict the transient side effect of IL-2 injections on the effector Tconv response. In silico results suggested that a combination of IL-2 and adoptive Treg transfer therapies can limit this side effect.

Relationship between intestinal mucosal barrier function and TLR9 expression and T cell subsets in patients with acute severe pancreatitis

Relationship between intestinal mucosal barrier function and TLR9 expression and T cell subsets in patients with acute severe pancreatitis

Levels and Clinical Significance of Regulatory B Cells and T Cells in Acute Myeloid Leukemia.

Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy, whose immunological mechanisms are still partially uncovered. Regulatory B cells (Bregs) and CD4+ regulatory T cells (Tregs) are subgroups of immunoregulatory cells involved in modulating autoimmunity, inflammation, and transplantation reactions. Herein, by studying the number and function of Breg and Treg cell subsets in patients with AML, we explored their potential role in the pathogenesis of AML. Newly diagnosed AML patients, AML patients in complete remission, and healthy controls were enrolled. Flow cytometry was used to detect percentages of Bregs and Tregs. ELISA was conducted to detect IL-10 and TGF-β in plasma. The mRNA levels of IL-10 and Foxp3 were measured with RT-qPCR. The relationship of Bregs and Tregs with the clinicopathological parameters was analyzed. There was a significant reduction in the frequencies of Bregs and an increase of Tregs in newly diagnosed AML patients compared with healthy controls. Meanwhile, patients in complete remission exhibited levels of Bregs and Tregs comparable to healthy controls. Furthermore, compared with healthy controls and AML patients in complete remission, newly diagnosed AML patients had increased plasma IL-10 but reduced TGF-β. IL-10 and Foxp3 mRNA levels were upregulated in the newly diagnosed AML patients. However, there were no significant differences in IL-10 and Foxp3 mRNA levels between patients in complete remission and healthy controls. Bregs and Tregs have abnormal distribution in AML patients, suggesting that they might play an important role in regulating immune responses in AML.

The role of T cells in pemphigus vulgaris and bullous pemphigoid.

Pemphigus vulgaris (PV) and bullous pemphigoid (BP) are autoantibody-mediated diseases clinically characterized by blistersanderosions of skin and/or mucous membranes. Immune imbalance and antibody generation are the key pathologies of autoimmune bullous diseases. Recently, a large number of studies have shown that T cell subsets, which are critical players in autoimmunity, exhibit a range of abnormalities and drive immunopathogenesis and skin inflammation in PV and BP. T helper (Th)1 cells mediate pro-inflammatory or immune responses through IFN-γ and Th2-derived cytokines, such as IL-4, can promote B cell proliferation, antibody production and immunoglobulin class-switching. Th17 cells promote inflammatory response and skin damage, while regulatory T cells suppress autoreactive CD4+ T cell activation and help control inflammation. T follicular helper cells cross-talk with B cells and facilitate autoantibody production. In this review, we discuss the immune features of PV and BP, with a focus on the aberrations in T cell subsets, such as Th1 cells, Th2 cells, Th17 cells, regulatory T cells, T follicular helper cells, CD8+ T cells, γδ T cells and resident memory T cells in the pathogenesis of PV and BP. Improved understanding of biological and immunological functions of T cell subsets in patients with autoimmune skin disorders will offer unique opportunities for the recognition of treatment targets for these complex diseases.

Low-Dose IL-2 for Treating Moderate to Severe Alopecia Areata: A 52-Week Multicenter Prospective Placebo-Controlled Study Assessing its Impact on T Regulatory Cell and NK Cell Populations

Low-Dose IL-2 for Treating Moderate to Severe Alopecia Areata: A 52-Week Multicenter Prospective Placebo-Controlled Study Assessing its Impact on T Regulatory Cell and NK Cell Populations

Quantitative multiplex immunofluorescence analysis identifies infiltrating PD1+ CD8+ and CD8+ T cells as predictive of response to neoadjuvant chemotherapy in breast cancer.

BackgroundThis study aimed to explore the potentially predictive role and dynamic changes of immune checkpoints on T cell subsets in patients with breast cancer receiving neoadjuvant chemotherapies.MethodsFluorescent multiplex immunohistochemistry (mIHC) was used to stain CD4, CD8, PD1, TIM3, and cytokeratins simultaneously in paired breast cancer samples before and after neoadjuvant therapies (NAT) in a prospective cohort (n = 50). Singleplex IHC was conducted to stain for CD3 in 100 cases with inclusion of extra retrospective 50 cases. Cell levels were correlated with clinicopathological parameters and pathological complete response (pCR).ResultsIn pretreatment tumors, the percentages of infiltrating CD8+, PD1+, PD1+CD8+, and the ratio of PD1+CD8+/CD8+ cells, were higher in pCR than non‐pCR patients in either the stromal or intratumoral area, but PD1+CD4+, TIM3+CD4+, TIM3+CD8+ cells and CD4+/CD8+ ratio was not. Multivariate analyses showed that the percentage of intratumoral CD8+ cells (OR, 1.712; 95% CI: 1.052–2.786; P = 0.030) and stromal PD1+CD8+/CD8+ ratio (OR, 1.109; 95% CI: 1.009–1.218; P = 0.032) were significantly associated with pCR. Dynamically, reduction in the percentages of PD1+, CD8+ and PD1+CD8+ cells after therapy strongly correlated with pCR. Notably, incremental percentages of PD1+CD8+ cells, rather than TIM3+CD8+, were shown in tumors from non‐pCR patients after NAT. CD3 staining confirmed the percentage of T cells were associated with pCR.ConclusionsPD1+CD8+ rather than TIM3+CD8+ cells are main predictive components within tumor‐infiltrating T cells in NAT breast cancer patients. Dynamically incremental levels of PD1+CD8+ cells occurred in non‐pCR cases after NAT, suggesting the combination of chemotherapy with PD1 inhibition might benefit these patients.Key pointsSignificant findings of the study PD1+CD8+, rather than TIM3+CD8+, T cells are the main component to predict the response of neoadjuvant therapies in breast cancer. What this study adds Incremental levels of PD1+CD8+ T cells in non‐pCR post‐NAT tumors suggest PD1 inhibition might benefit in the neoadjuvant setting.

1126P Prediction of clinical outcome by soluble immune checkpoints and T cell subsets in patients treated with immune checkpoint blockers for metastasized melanoma

1126P Prediction of clinical outcome by soluble immune checkpoints and T cell subsets in patients treated with immune checkpoint blockers for metastasized melanoma

Systemic Sclerosis Perturbs the Architecture of the Immunome.

Systemic sclerosis (SSc) is an autoimmune disease characterized by excessive fibrosis of skin and internal organs, and vascular dysfunction. Association of T and B cell subsets has been reported in SSc; however, there is lack of systematic studies of functional relations between immune cell subsets in this disease. This lack of mechanistic knowledge hampers targeted intervention. In the current study we sought to determine differential immune cell composition and their interactions in peripheral blood of SSc patients. Mononuclear cells from blood of SSc patients (n = 20) and healthy controls (n = 10) were analyzed by mass cytometry using a 36-marker (cell surface and intracellular) panel. Transcriptome analysis (m-RNA sequencing) was performed on sorted T and B cell subsets. Unsupervised clustering analysis revealed significant differences in the frequencies of T and B cell subsets in patients. Correlation network analysis highlighted an overall dysregulated immune architecture coupled with domination of inflammatory senescent T cell modules in SSc patients. Transcriptome analysis of sorted immune cells revealed an activated phenotype of CD4 and mucosal associated invariant T (MAIT) cells in patients, accompanied by increased expression of inhibitory molecules, reminiscent of phenotype exhibited by functionally adapted, exhausted T cells in response to chronic stimulation. Overall, this study provides an in-depth analysis of the systemic immunome in SSc, highlighting the potential pathogenic role of inflammation and chronic stimulation-mediated “functional adaptation” of immune cells.

Characterization of the DNAM-1, TIGIT and TACTILE Axis on Circulating NK, NKT-Like and T Cell Subsets in Patients with Acute Myeloid Leukemia.

Background: Acute myeloid leukemia (AML) remains a major clinical challenge due to poor overall survival, which is even more dramatic in elderly patients. TIGIT, an inhibitory receptor that interacts with CD155 and CD112 molecules, is considered as a checkpoint in T and NK cell activation. This receptor shares ligands with the co-stimulatory receptor DNAM-1 and with TACTILE. The aim of this work was to analyze the expression of DNAM-1, TIGIT and TACTILE in NK cells and T cell subsets in AML patients. Methods: We have studied 36 patients at the time of diagnosis of AML and 20 healthy volunteers. The expression of DNAM-1, TIGIT and TACTILE in NK cells and T cells, according to the expression of CD3 and CD56, was performed by flow cytometry. Results: NK cells, CD56− T cells and CD56+ T (NKT-like) cells from AML patients presented a reduced expression of DNAM-1 compared with healthy volunteers. An increased expression of TIGIT was observed in mainstream CD56− T cells. No differences were observed in the expression of TACTILE. Simplified presentation of incredibly complex evaluations (SPICE) analysis of the co-expression of DNAM-1, TIGIT and TACTILE showed an increase in NK and T cells lacking DNAM-1 and co-expressing TIGIT and TACTILE. Low percentages of DNAM-1−TIGIT+TACTILE+ NK cells and DNAM-1− TIGIT+TACTILE+ CD56− T cells were associated with a better survival of AML patients. Conclusions: The expression of DNAM-1 is reduced in NK cells and in CD4+ and CD8+ T cells from AML patients compared with those from healthy volunteers. An increased percentage of NK and T cells lacking DNAM-1 and co-expressing TIGIT and TACTILE is associated with patient survival, supporting the role of TIGIT as a novel candidate for checkpoint blockade.

Absolute reduction of peripheral regulatory T cell in patients with relapsing polychondritis

Although relapsing polychondritis (RP) is considered as an immune-mediated systemic disease, the levels of peripheral lymphocyte subpopulations are rarely studied in patients with RP. In this study, we focused on changes of peripheral CD4+T cell subsets in patients with RP. Absolute numbers and percentages of CD4+T cell subsets including helper T(Th)1, Th2, Th17 cells and regulatory T (Treg) cells in peripheral blood (PB) from 19 RP patients, healthy controls and RA patients respectively were assessed by flow cytometry combined a microbead-based single-platform method. We compared the CD4+T cell levels in all RP patients and healthy controls. In addition, we analysed the difference of the absolute number and percentage of Treg cells between RP and RA patients. Compared with healthy controls, all RP patients had significantly both lower absolute number and proportion of Treg cells (absolute number, 45.10/μl vs. 22.48/μl, p<0.001; proportion, 5.19% vs. 3.78%, p<0.001) no matter whether they had received treatment or not. Similarly, the absolute number of Th2 cells in all RP patients was decreased (10.19/μl vs. 7.44/μl, p=0.030). However, there were no significant differences in percentages and absolute numbers of Th1 and Th17 cells between RP patients and healthy controls. The above results led to increased ratios of Th1/Treg (3.68 vs. 2.06, p=0.020), Th2/Treg (0.29 vs. 0.21, p=0.037) and Th17/Treg (0.25 vs. 0.14, p<0.001) in RP patients, and untreated RP patients were mainly characterised by the imbalance of Th17/Treg (0.25 vs. 0.14, p<0.01). There was no significant difference in Treg cells between RP and RA patients (p>0.05). Our data suggest that the reduction of Treg cells and its imbalance with Th cells play an important role in the pathogenesis of RP.

Lymphocyte activation gene 3 expression on T lymphocyte cell subsets in patients with myelodysplastic syndrome

Objective: To investigate the expression of Lymphocyte activation gene 3 (LAG3) in myelodysplastic syndromes (MDS) patients. Methods: A total of 16 MDS patients newly diagnosed in Hematology Department of Tianjin Medical University were enrolled from January to November 2019. The healthy control (HC) group includes 16 cases of healthy adults. The expression levels of LAG3 on CD8(+)T cells, CD4(+)T cells and regulatory T cells (Treg) in MDS patients and healthy controls were detected by flow cytometry. Results: A total of 16 patients with MDS were included, including 5 males and 11 females, with a median age of 56 (18-80) years old. HC group includes 16 healthy adults, 8 men and 8 women, with a median age of 40 (17-69) years. There was no statistically significant difference in gender and age composition between the two groups (both P>0.05). The expression of LAG3 on CD8(+)T cells in MDS patients (74.45%±22.31%) was significantly higher than that in HC group (58.78%±14.82%, P<0.05). The LAG3 expression on Treg in MDS patients (64.91%±10.32%) were significantly higher than that of HC group (49.09%±13.58%, P<0.05). There was no statistical difference in LAG3 expression on CD4(+)T cells between the two groups. Conclusion: The expression of LAG3 on CD8(+)T cells and Treg increases in MDS patients than that of healthy people.

Characteristics of Circulating CD4+ T Cell Subsets in Patients with Mycobacterium avium Complex Pulmonary Disease.

Although prevalence of Mycobacterium avium complex pulmonary disease (MAC-PD) is increasing, limited data are available regarding vulnerability to Mycobacterium avium complex (MAC) infections. To understand the pathobiology of interaction between MAC and host-immunity, it is important to understand the characteristics for circulating T cells in terms of the immunological phenotype and functional correlates in MAC-PD. We aimed to characterize immunophenotype, cytokine profile, and immune inhibitory receptors of circulating CD4+ T cells in MAC-PD patients. We enrolled 71 MAC-PD and 20 control individuals. Flow cytometric analysis was performed to determine T cell subsets and immune checkpoint markers. Ex vivo cytokine productions in response to MAC were determined using enzyme-linked immunosorbent assay. The frequencies of CD4+ T cells and CD4+IL-17+ T cells decreased, while CD4+IL-4+ T cells and CD4+CD25+Foxp3+ T cells increased in peripheral blood mononuclear cells (PBMCs) of MAC-PD individuals upon MAC stimulation compared with those cells in healthy donor-PBMCs. Additionally, we found increased PD-1, CTLA-4, and TIM-3-expressing T cells in MAC- PD individuals in response to MAC-stimulation, indicating that suppressed T cell-mediated response is associated with the susceptibility to MAC infection. These results may help to explain impaired T cell-mediated responses and pave the way for better strategies to achieve protective immunity against MAC infection.

Correlation of vitamin D with inflammatory factors, oxidative stress and T cell subsets in patients with autoimmune hepatitis.

Correlation of vitamin D with inflammatory factors, oxidative stress and T cell subsets in patients with autoimmune hepatitis were investigated. Patients with liver diseases (n=635) treated in The Sixth People's Hospital of Qingdao City from March 2015 to January 2018 were selected, among which 80 cases diagnosed with autoimmune hepatitis were included into observation group, and 80 healthy cases were included into control group. Patients with autoimmune hepatitis were further divided into normal 25-hydroxyvitamin D [25-(OH) D] group (n=40) and abnormal 25-(OH) D group (n=40) according to the level of 25-(OH) D, and divided into normal liver function group (n=40) and abnormal liver function group (n=40). 25-(OH) D, liver function, inflammatory factors, oxidative stress level and T cell subsets were compared. In the observation group, levels of 25-(OH) D, superoxide dismutase (SOD), total antioxidant capacity, and T cell subsets were lower than those in the control group (P<0.05), while levels of total bilirubin (TBIL), indirect BIL (IBIL), direct BIL (DBIL), aspartate aminotransferase (AST), alanine aminotransferase (ALT), inflammatory factors and malondialdehyde (MDA) were higher than those in the control group (P<0.05). In the normal 25-(OH) D group, levels of inflammatory factors and oxidative stress factor were lower than those in the abnormal 25-(OH) D group (P<0.05), while the SOD level, total antioxidant capacity and T cell subset counts were higher than those in the abnormal 25-(OH) D group (P<0.05). Moreover, the 25-(OH) D level in patients with autoimmune hepatitis was negatively correlated with hs-CRP, tumor necrosis factor-α (TNF-α), ALT and MDA, but positively correlated with CD3+ and CD4+ counts, SOD and total antioxidant capacity. Patients with autoimmune hepatitis, especially those with decreased level of vitamin D, are more prone to enhanced inflammatory and stress responses, decreased levels of T cell subsets and decline in immunity.

Imbalance in B cell and T Follicular Helper Cell Subsets in Pulmonary Sarcoidosis

Sarcoidosis is a systemic granulomatous disease that develops due to the Th1, Th17 and Treg lymphocytes disturbance. There is an assumption, that B cells and follicular T-helper (Tfh) cells may play an important role in this disorder, as well as in several other autoimmune diseases. The aim of this study was to determine CD19+ B cells subset distribution in the peripheral blood and to define disturbance in the circulating Tfh cells subsets in patients with sarcoidosis. The prospective comparative study was performed in 2016–2018, where peripheral blood B cell subsets and circulating Tfh cell subsets were analyzed in 37 patients with primarily diagnosed sarcoidosis and 35 healthy donors using multicolor flow cytometry. In the results of our study we found the altered distribution of peripheral B cell subsets with a predominance of “naïve” (IgD + CD27−) and activated B cell (Bm2 and Bm2′) subsets and a decreased frequency of memory cell (IgD+ CD27+ and IgD− CD27+) in peripheral blood of sarcoidosis patients was demonstrated. Moreover, we found that in sarcoidosis patients there are increased levels of B cell subsets, which were previously shown to display regulatory capacities (CD24+++ CD38+++ and CD5 + CD27−). Next, a significantly higher proportion of CXCR5-expressing CD45RA − CCR7+ Th cells in patients with sarcoidosis in comparison to the healthy controls was revealed, that represents the expansion of this memory Th cell subset in the disease. This is the first study to demonstrate the association between the development of sarcoidosis and imbalance of circulating Tfh cells, especially CCR4− and CXCR3-expressing Tfh subsets. Finally, based on our data we can assume that B cells and Tfh2- and Tfh17-like cells – most effective cell type in supporting B-cell activity, particularly in antibody production – may be involved in the occurrence and development of sarcoidosis and in several other autoimmune conditions. Therefore, we can consider these results as a new evidence of the autoimmune mechanisms in the sarcoidosis development.

T cell metabolism: new insights in systemic lupus erythematosus pathogenesis and therapy.

T cell subsets are critically involved in the development of systemic autoimmunity and organ inflammation in systemic lupus erythematosus (SLE). Each T cell subset function (such as effector, helper, memory or regulatory function) is dictated by distinct metabolic pathways requiring the availability of specific nutrients and intracellular enzymes. The activity of these enzymes or nutrient transporters influences the differentiation and function of T cells in autoimmune responses. Data are increasingly emerging on how metabolic processes control the function of various T cell subsets and how these metabolic processes are altered in SLE. Specifically, aberrant glycolysis, glutaminolysis, fatty acid and glycosphingolipid metabolism, mitochondrial hyperpolarization, oxidative stress and mTOR signalling underwrite the known function of T cell subsets in patients with SLE. A number of medications that are used in the careof patients with SLE affect cell metabolism, and the development of novel therapeutic approaches to control the activity of metabolic enzymes in T cell subsets represents a promising endeavour in the search for effective treatment of systemic autoimmune diseases.

Mitophagy Balance in Various Cell Subsets in Patients with ANCA-Associated Vasculitis and Correlation with the Presence of Anti-Neutrophil Cytoplasmic Antibodies.

ANCA-associated vasculitides (AAVs) are characterised by heterogeneous molecular and pathophysiological traits, causing ambiguous differential diagnosis and taxonomy. Response to therapy has proven far from successful, contributing to high mortality. Transcriptome analysis of different vasculitis subtypes adds new leads in elucidating mechanisms of disease and the role of specific cell subsets to them. Recent findings have shown that mitophagy is a procedure whose imbalance could lead to immune dysregulation with certain involvement to autoimmunity. Inflammatory response related mitophagy is yet to be described in AAVs. We here describe a research protocol to investigate mitophagy in monocytes, neutrophils, and T cells in AAV patients, and the relationship of disturbed mitophagy with ANCA seropositivity.

Abstract B45: IL35/STAT3 axis as regulator of tolerance and T-cell exclusion in pancreatic cancer

Abstract Pancreatic ductal adenocarcinoma (PDA) is an aggressive malignancy refractory to immunotherapeutic interventions. The mechanisms that drive robust immunosuppression and CD8+ T-cell dysfunction in PDA are not well known. Using the Kras- and p53-driven mouse model of pancreatic cancer, we show that activation of IL35/STAT3 pathways directs reprogramming of suppressive regulatory B-cell lineage and inhibits CD8+ T cells via suppression of gene program that regulates infiltration and effector function. Activation of STAT3 in CD8+ T cells is driven by B cell, but not Treg-specific production of cytokine IL35. Targeting IL35 via cell lineage-specific deletion or therapeutic anti-IL35 blockade converts PDA from CD8+ T cell low to high tumor and confers sensitivity to anti-PD1 immunotherapy. Therapeutic inhibition of STAT signaling in tumor-educated CD8+ T cells improves PDA growth control upon adoptive transfer to tumor-bearing animals. Finally, we identify IL35+ B cell subset in patients with PDA and demonstrate that the presence of IL35+ cells in tumor samples predicts increased occurrence of dysfunctional CD8+ T cells. Together, these data identify IL35/STAT3 signaling as an important mediator of immune tolerance and a direct link to CD8+ T-cell exclusion and immunotherapy resistance in PDA. Citation Format: Bhalchandra Mirlekar, Daniel Michaud, Yuliya Pylayeva-Gupta. IL35/STAT3 axis as regulator of tolerance and T-cell exclusion in pancreatic cancer [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; 2019 Sept 6-9; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2019;79(24 Suppl):Abstract nr B45.

Molecular Signatures of Dengue Virus-Specific IL-10/IFN-γ Co-producing CD4 T Cells and Their Association with Dengue Disease

SUMMARYDengue virus (DENV) can cause diseases ranging from dengue fever (DF) to more severe dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). Whether antiviral T cells contribute to the protection against or pathogenesis of severe disease is not well defined. Here, we identified antigen-specific IL-10+IFN-γ+ double-positive (DP) CD4 T cells during acute DENV infection. While the transcriptomic signatures of DP cells partially overlapped with those of cytotoxic and type 1 regulatory CD4 T cells, the majority of them were non-cytotoxic/Tr1 and included IL21, IL22, CD109, and CCR1. Although we observed a higher frequency of DP cells in DHF, the transcriptomic profile of DP cells was similar in DF and DHF, suggesting that DHF is not associated with the altered phenotypic or functional attributes of DP cells. Overall, this study revealed a DENV-specific DP cell subset in patients with acute dengue disease and argues against altered DP cells as a determinant of DHF.

Intestinal microbiota composition and peripheral blood Th cell subsets in patients with multiple sclerosis

At present, the role of intestinal microbiota in diverse diseases of the central nervous system, including of multiple sclerosis (MS) has been extensively investigated. Self-reactive CD4+ Th1 and Th17 cells specific to myelin-derived antigens play a key role in the MS pathogenesis. Taking into consideration pathogenetic features related to MS development, we examined a relation between intestinal microbiocenosis and abundance of various peripheral blood helper T (Th) cell subsets in MS patients. Objective of the study: to assess prevalence of individual members of the intestinal microbiota in MS patients and analyze a relation with peripheral blood Th cell subsets. Prevalence of symbiotic and opportunistic microbial species was estimated by bacteriological method and real time PCR in 112 MS patients (72 females, 40 males) of varying severity and duration. Th cell subsets (Th1, Th2, Th17, Th1/Th17, Th17/Th22, DP Th17) were analyzed by using multi-color flow cytometry based on Th cell subset-specific surface expression of chemokine receptors. A relationship between individual intestinal microbiota species and severity, duration and rate of MS progression, as well as with the phenotype of immune cells was assessed. It was found that the most significant correlation between percentage of peripheral blood Th cell subsets was observed with prevalence of Lactobacillus spp., Enterococcus spp. and Enterobacter spp. Moreover, prevalence of Enterococcus spp. Th cell composition influenced synergistically or antagonistically together with Enterobacter spp. or Lactobacillus spp., respectively. It is suggested that direct and indirect impact of intestinal microbiota composition on human immune system might contribute to developing novel strategies for treating MS.

Effect of tripterygium glycosides on serum IL-6, IL-8 and T cell subsets in patients with chronic glomerulonephritis

Objective To explore the effects of tripterygium glycosides on serum interleukin-6 (IL-6), interleukin-8 (IL-8) and T cell subsets in patients with chronic glomerulonephritis. Methods A total of 102 patients with chronic glomerulonephritis admitted to the hospital between August 2016 and August 2018 were enrolled and divided into a control group and an experimental group according to the single-blind method, with 51 cases in each group. Conventional therapy was carried out in both groups, with tripterygium glycosides given additionally to the experimental group. After 3 months of continuous treatment, the clinical efficacy, serum IL-6, IL-8, T cell subsets, renal function and adverse reactions were compared between the two groups. Results The total effective rate of treatment in the experimental group was higher than that in the control group, and the difference was statistically significant (P 0.05). Conclusions For patients with chronic glomerulonephritis, tripterygium glycosides combined with conventional therapy is with great safety, which can help improve the clinical efficacy, and the patients’ renal function and immune function, and reduce the levels of serum IL-6 and IL-8, without increasing adverse reactions. Key words: Glomerulonephritis; TRIPTERYGIUM WILFORDII; Interleukin-6; Interleukin-8; T-Lymphocyte Subsets