T cell receptor (TCR) signaling by MHC class I and II induces thymocytes to acquire cytotoxic and helper fates via the induction of Runx3 and ThPOK transcription factors, respectively. The mechanisms by which TCR signaling is translated into transcriptional programs for each cell fate remain elusive. Here, we show that, in post-selection thymocytes, a genome organizer, SATB1, activates genes for lineage-specifying factors, including ThPOK, Runx3, CD4, CD8, and Treg factor Foxp3, via regulating enhancers in these genes in a locus-specific manner. Indeed, SATB1-deficient thymocytes are partially re-directed into inappropriate T lineages after both MHC class I- and II-mediated selection, and they fail to generate NKT and Treg subsets. Despite its essential role in activating enhancers for the gene encoding ThPOK in TCR-signaled thymocytes, SATB1 becomes dispensable for maintaining ThPOK in CD4+ T cells. Collectively, our findings demonstrate that SATB1 shapes the primary T cell pool by directing lineage-specific transcriptional programs in the thymus.

The host immune response could be an imperative factor in the pathogenesis of neurosyphilis, but the role of T lymphocyte subsets remains unclear. In the present study, we assessed the CD4+ T and CD8+ T cell subsets in the peripheral blood of patients with HIV-negative symptomatic neurosyphilis and then explored the clinical application value of neurosyphilis.

This study aims to compare the proportion of peripheral blood T lymphocyte subsets and related blood cell and bone marrow cytology indexes between patients with aplastic anemia (AA) and hypoplastic myelodysplastic syndrome (hypo-MDS), and investigate the clinical identification significance.

The aim of this study is to evaluate the age related changes of T lymphocyte subsets in C57BL/6 mice and immune function. Multi-color immunofluorescence techniques that were used to analyse relative numbers of T lymphocyte subsets include CD4+, CD8+, naive and memory CD4+ and CD8+, CD8+CD28+ T cells in peripheral blood of C57BL/6 mice from different age groups (Group I: 2 months old; Group II: 7 months old; Group III: 21 months old); Splenocytes isolated from different group mice were stimulated with Con A to evaluate the proliferative ability. Compared with group I, group II had a significant reduction in the percentage of CD4+, naive CD4+ and CD8+ T cells and an increase in the percentage of CD8+ T cells, while group III had a significant reduction in the percentage of CD4+, naive CD4+ and CD8+ T cells and increase in the percentage of CD8+, memory CD4+ and CD8+ T cells in peripheral blood. Compared with group II, group III had a significant reduction in the percentage of naive CD8+ T cells and increase in the percentage of memory CD4+ and CD8+, CD8+CD28+ T cells in peripheral blood. The T lymphocyte proliferation in vitro showed that groups II and III had a lower proliferative capacity than group I, between groups II and III, there was not a significant difference. We provide relative values for the T lymphocyte subsets in the different age groups of C57BL/6 mice. The immune system began aging at 7 months old in C57BL/6 mice under a specific pathogen free environment.

A high incidence of viral persistence and progression to chronic hepatitis are characteristic features of hepatitis C virus (HCV) infection. Since T lymphocytes play a critical role in virus clearance, their abnormalities in undergoing apoptosis may cause the insufficient antiviral immune responses leading to persistent viral infection. Recent reports have suggested that monocyte-dependent cell death (MDCD) is a mechanism of T lymphocyte apoptosis in chronic viral infection. The current study was designed to monitor apoptosis of CD4+ and CD8+ T lymphocyte subsets in co-culture with CD14+ monocytes under the apoptotic stimuli in patients with chronic hepatitis C. Cell mortalities of CD4+ and CD8+ T lymphocyte subsets from patients exhibiting various degrees of chronic hepatitis C were increased to a greater extent when incubated with CD14+ monocyte subset in medium containing phorbol 12-myristate 13-acetate. The current observations demonstrate that MDCD of CD4+ and CD8+ T lymphocyte subsets may provide a cellular basis for immune dysfunction which results in insufficient viral clearance and progression of liver disease in chronic HCV infection.

Background: T-lymphocyte subsets reflect patients' immune status and are associated with adverse outcomes in various diseases. However, the association between T-lymphocyte subsets and major infection and renal outcome in chronic kidney disease (CKD) patients has not been well-addressed. Methods: Patients diagnosed with stage 3-5 of non-dialysis CKD were recruited, and healthy subjects were selected as the controls. T-lymphocyte subsets (CD3+, CD4+, CD8+) were detected by flow cytometry, and the CD4+/CD8+ T cell ratio was then calculated. Patients were divided into the normal-level group and the low-level group according to the clinical reference value. The primary outcomes were the major infection and renal outcome. Results: A total of 410 CKD patients were enrolled; the average age was 47.25 years. Compared to the healthy controls, the level of CD3+, CD4+, CD8+ T cells, and the CD4+/CD8+ T cell ratio were significantly decreased in CKD patients (p < 0.05). During the median follow-up of 2.56 (quartile interval 1.24-3.46) years, major infections occurred in 15.10% of the CKD patients. The incidence of infection was significantly higher in the low-level group of CD3+, CD4+ T cells, and CD4+/CD8+ T cell ratio compared with the normal level groups. Kaplan-Meier analysis showed that the lower level of CD3+, CD4+ T cells, and CD4+/CD8+T cell ratio is associated with a greater risk of infection. Cox regression analysis further confirmed that low CD3+, CD4+ T cells, and CD4+/CD8+ T cell ratio were independent risk factors of infection in CKD patients. Moreover, during the follow-up, renal events occurred in 37.50% of patients. Kaplan-Meier analysis indicated that low levels of CD3+, CD4+, and CD8+ T cells are significantly associated with renal outcome in CKD patients. Cox regression analysis showed that low level of CD3+ T cells (HR = 2.407, 95% CI: 1.664-3.482, p < 0.001), CD4+ T cells (HR = 2.397, 95% CI: 1.633-3.518, p < 0.001) and CD8+ T cells (HR = 2.416, 95% CI: 1.476-3.955, p < 0.001) were independent risk factors for renal outcome after multivariable-adjusted. Conclusion: CKD patients had a defect in T-lymphocyte subpopulation. T-lymphocyte subsets were closely associated with infection and renal outcome in CKD patients. Suggesting T-lymphocyte subsets are independent predictors of infection and renal outcome in CKD patients.

CD4+ T lymphocytes play crucial roles in the adaptive immune system. CD4, as the most effective marker to delineate the T-helper subsets, was identified in many fish species. Two CD4 homologs, CD4-1 and CD4-2, have been reported in flounder (Paralichthys olivaceus). In this study, monoclonal antibodies (mAbs) against CD4-1 and CD4-2 of flounder were produced, CD4+ T lymphocytes were isolated and identified, and the variations in CD4+ and CD8+ T lymphocytes and IgM+ B lymphocytes after Poly I:C, PMA or β-glucan stimulation were investigated. Then, the expression of transcription factors and cytokines in sorted CD4+ T lymphocytes was analyzed. The results showed that the mAbs were specific to flounder CD4-1+ and CD4-2+ T cells. CD4-1+ and CD4-2+ cells responded to all three stimulants, while CD8+ T lymphocytes only give a strong response to Poly I:C, and the percentages of IgM+ B lymphocytes showed a tendency to increase. After stimulation, the expression of transcription factors and cytokines of Th1, Th2 and Th17 cells varied in CD4+ T cells. These results will provide crucial foundations for the differentiation and function of teleost CD4+ T lymphocytes.

Osteosarcoma (OS) is the most common malignant bone tumor, which often has lung metastasis. The survival rate after tumor metastasis is very low. Treatments including the antitumor immunocompetence of innate immune cells are found favorable for OS tumor. However, as a major means of early tumor detection, there are still few studies on T cells in peripheral blood of OS patients.

Immune profiles in endometrium may be changed in patients with IVF failure and its possible correlations with immune parameters in peripheral blood are important for the diagnostic approach. Such correlations in healthy women are unknown and have been studied in the present research. The expression of CD56, CD158a, HLA DR, CD69 in T lymphocytes, CD4 T lymphocytes, CD8+ T lymphocytes and NK cells were studied by flow-cytometry in endometrium and peripheral blood in healthy 24 donors of oocytes aged 25-32 years. Levels of T lymphocyte and T helper cells were lower in endometrium and no differences in CD8 T lymphocytes were registered between endometrium and peripheral blood. The expression of HLA DR and especially CD69 was higher in CD3, CD4, CD8 T cells in endometrium in comparison with peripheral blood. The endometrium lymphocyte population was enriched by NK cells that were generally CD56++ with a higher expression of HLA DR and almost in total were CD69 positive. Strong positive correlations of CD8 expression in NK cells (r = 0.6478, p < 0.001) and HLA DR expression in CD8 T cells (r = 0.6107, p < 0.01) between peripheral blood and endometrium were registered in fertile women. The endometrial CD56 expression in CD8+ T cells negatively correlated with endometrial CD8 expression in NK cells (r = -0.5252, p < 0.01) which possibly reflected a suppressive and regulating mechanism in the endometrium. CD8+ NK cells and HLA DR+ CD8 T cells in endometrium were related to the same subsets in peripheral blood.

Radiation therapy (RT) induces an immune response, but the relationship of this response with tumor type is not fully understood. This meta-analysis further elucidated this relationship by analyzing the changes in T lymphocyte subsets in different tumors before and after radiotherapy.

Immune thrombocytopenia (ITP) is an acquired autoimmune disease. This study's objective was to estimate the variations in the population of CD4+CD25+High FoxP3+ cells (CD4+ regulatory T-lymphocytes; Tregs) in previously untreated children with chronic ITP managed in Assiut University Hospitals, as well as to evaluate the efficacy of high-dose dexamethasone (HD-DXM) in these patients.

Different lipid sources differ in the fatty acid profiles and differently affect growth performance as well as immune function of broilers. The influences of different dietary lipid sources on growth performance, nutrient digestibility, blood T lymphocyte population, and cardiac antioxidant status were investigated of broilers. A total of 360 one-day-old male broilers (BW = 44 ± 3 g) were randomized into 3 treatment groups, consisting of 6 replicates with 20 birds in each group. Broilers received standard diets supplemented with 5% (wt/wt) of lard (LD, as a control diet), sesame oil (SO), or flaxseed oil (FO). Broilers in both SO and FO treatment groups had lower (P < 0.05) feed conversion ratios from 22 to 42 d and during the overall phase compared to those in LD treatment group. Meanwhile, the apparent total tract nutrient digestibility of crude fat in SO and FO treatment groups was higher than that in LD treatment group. Both FO and SO treatments decreased (P < 0.05) abdominal fat percentage compared to LD treatment. Total triglycerides and total cholesterol in chicken blood were decreased (P < 0.05) by SO and FO treatments compared to LD treatment. Feeding broilers with FO and SO led to a decrease (P < 0.05) in blood CD4+ T lymphocyte count and in CD4+:CD8+ ratio compared to LD treatment. Sesame oil and FO treatments increased cardiac glutathione peroxidase (P < 0.05) compared to LD treatment. It is concluded that addition of 5% SO and FO to the standard corn-soybean meal diet improved feed efficiency, increased the activities of cardiac glutathione peroxidase, and affected the T lymphocytes ratio of fast growing broilers.

Diabetic neuropathic pain is a common and devastating complication of type 1 diabetes, but the mechanism by which it develops and persists is yet to be fully elucidated. This study utilised high-dimensional suspension mass cytometry in a pilot cohort to investigate differences in peripheral blood immunophenotypes between type 1 diabetes patients with (n ​= ​9) and without (n ​= ​9) peripheral neuropathic pain. The abundance and activation of several leukocyte subsets were investigated with unsupervised clustering approaches FlowSOM and SPADE, as well as by manual gating. Major findings included a proportional increase in CD4+ central memory T cells and an absolute increase in classical monocytes, non-classical monocytes, and mature natural killer cells in type 1 diabetes patients with pain compared to those without pain. The expression of CD27, CD127, and CD39 was upregulated on select T cell populations, and the phosphorylated form of pro-inflammatory transcription factor MK2 was upregulated across most populations. These results provide evidence that distinct immunological signatures are associated with painful neuropathy in type 1 diabetes patients. Further research may link these changes to mechanisms by which pain in type 1 diabetes is initiated and maintained, paving the way for much needed targeted treatments.

The aim of the present study was to observe the immune mechanism underlying the rejection of chemically extracted acellular nerve allografts for use in clinical applications. A total of 128 BALB/c mice were randomly divided into a negative contrast group (NC, 32 mice), a fresh autograft group (AG, 32 mice), a fresh allogeneic nerve group (FN, 32 mice) and a chemically extracted acellular allogeneic nerve group (CEN, 32 mice). Various types of nerve grafts were implanted into the thigh muscle of BALB/C mice in the corresponding groups. At 3, 7, 14 and 28 days post-operation, the mice (8 cases from each group) were sacrificed and their spleens were extracted. The spleens were ground into paste. The erythrocytes and other cells were lysed using distilled water and the T lymphocytes were collected. Monoclonal antibodies (CD3, CD4, CD8, CD25, IL-2, IFN-γ and TNF-α) were then added to the solution. The Facial Action Coding System was used to determine the positive rates of the cells combined with the monoclonal antibodies above. No significant statistical differences were observed between the CEN, NC and AG groups. However, some data of the FN group were significantly higher than those of the other groups at the corresponding time. No obvious immune rejections were observed among the chemically extracted acellular nerve allografts compared with fresh nerve autograft.

CD4 and CD8 T lymphocyte activation requires the generation of sufficient energy to support new biosynthetic demands. Following T cell receptor (TCR) engagement, these requirements are met by an increased glycolysis, due, at least in part, to induction of the Glut1 glucose transporter. As Glut1 is upregulated on tumor cells in response to hypoxia, we assessed whether surface Glut1 levels regulate the antigen responsiveness of human T lymphocytes in both hypoxic and atmospheric oxygen conditions. Notably, Glut1 upregulation in response to TCR stimulation was significantly higher in T lymphocytes activated under hypoxic as compared to atmospheric oxygen conditions. Furthermore, TCR-stimulated human T lymphocytes sorted on the basis of Glut1-Lo and Glut1-Hi profiles maintained distinct characteristics, irrespective of the oxygen tension. While T cells activated in hypoxia divided less than those activated in atmospheric oxygen, Glut1-Hi lymphocytes exhibited increased effector phenotype acquisition, augmented proliferation, and an inverted CD4/CD8 ratio in both oxygen conditions. Moreover, Glut1-Hi T lymphocytes exhibited a significantly enhanced ability to produce IFN-γ and this secretion potential was completely dependent on continued glycolysis. Thus, Glut1 surface levels identify human T lymphocytes with distinct effector functions in both hypoxic and atmospheric oxygen tensions.

Immunofluorescence studies were carried out in cutaneous T cell lymphoma (mycosis fungoides) in order to analyse the microanatomical relationship of the different T lymphocyte subsets (inducer and suppressor/cytotoxic cell populations) to large nonlymphoid Langerhans-type and so-called "indeterminate" or interdigitating cells. The conventional and mouse (monoclonal) antibodies were used in various combinations using fluorescein and rhodamine labeled second layers. In 5 of the 7 cases studied the dermal infiltrate consisted of numerous T (HuTLA+) lymphocytes, 80-90% of which expressed the inducer phenotype (HuTLA+,OKT4+). Most of these cells formed close contact with large cells exhibiting large amounts of Ia-like antigens. These cells corresponded to the interdigitating and indeterminate cells in the sections. By contrast, only small numbers (10-20%) of T cells of suppressor/cytotoxic type (HuTLA+,OKT8+) were seen. These did not show a close affinity to the Ia-like antigen positive nonlymphoid component but appeared to have a predilection for the epidermis. Epidermal Langerhans cells, also strongly Ia-like antigen positive, were further defined by 2 monoclonal antibodies reacting with a cortical thymocyte antigen HTA-1. Although Langerhans cells are probably related to the Ia-like antigen positive dermal cells only a few of the abundant latter population were HTA-1+. In the remaining 2 cases, larger populations of OKT8+ (suppressor/cytotoxic) cells were seen and could be heralding a particularly benign course. These observations indicate a close functional relationship between the lymphoid and Ia-like antigen positive dermal cells during the pre-malignant phase of cutaneous T cell lymphoma.

The development of chronic obstructive pulmonary disease (COPD) is related to the T lymphocyte mediated inflammatory immune response and immune imbalance. The purpose of this systematic review was to evaluate the clinical efficacy and safety of acupoint application on T lymphocyte subsets in patients with COPD.

The composition of tumor-infiltrating lymphocytes (TIL) reflects biology and immunogenicity of cancer. Here, we characterize T-cell subsets and expression of immune checkpoint molecules in head and neck squamous cell carcinoma (HNSCC). We analyzed TIL subsets in primary tumors (n = 34), blood (peripheral blood mononuclear cells (PBMC); n = 34) and non-cancerous mucosa (n = 7) of 34 treatment-naïve HNSCC patients and PBMC of 15 healthy controls. Flow cytometry analyses revealed a highly variable T-cell infiltration mainly of an effector memory phenotype (CD45RA-/CCR7-). Naïve T cells (CD45RA+/CCR7+) were decreased in the microenvironment compared to PBMC of patients, while regulatory T cells (CD4+/CD25+/CD127low and CD4+/CD39+) were elevated. Furthermore, we performed digital image analyses of entire cross sections of HNSCC to define the 'Immunoscore' (CD3+ and CD8+ cell infiltration in tumor core and invasive margin) and quantified MHC class I expression on tumor cells by immunohistochemistry. Immune checkpoint molecules cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), programmed cell death 1 (PD-1) and programmed cell death 1 ligand 1 (PD-L1) were increased in TILs compared to peripheral T cells in flow-cytometric analysis. Human papillomavirus (HPV) positive tumors showed higher numbers of TILs, but a similar composition of T-cell subsets and checkpoint molecule expression compared to HPV negative tumors. Taken together, the tumor microenvironment of HNSCC is characterized by a strong infiltration of regulatory T cells and high checkpoint molecule expression on T-cell subsets. In view of increasingly used immunotherapies, a detailed knowledge of TILs and checkpoint molecule expression on TILs is of high translational relevance.

Immune responses play an important role in the pathogenesis of polycystic ovary syndrome (PCOS). However, the characteristics of T lymphocyte subsets in PCOS remain insufficiently understood. In this study, lymphocytes of follicular fluid (FF) were obtained from oocyte retrieval before in-vitro fertilization (IVF) in infertile women with or without PCOS. The levels of cluster of differentiation 25 (CD25), CD69, programmed death 1 (PD-1), interferon-γ (IFN-γ), interleukin 17A (IL-17A) and IL-10 in T lymphocytes were determined by flow cytometry. Our results showed that the percentage of FF CD8+ T cells was significantly decreased in infertile patients with PCOS (P < 0.05). Furthermore, the levels of CD69 and IFN-γ were significantly decreased and the level of PD-1 was increased in both CD4+ and CD8+ T cells from infertile patients with PCOS (P < 0.05). Moreover, the expression of PD-1 on CD4+ or CD8+ T cells was positively correlated with the estradiol (E2) levels in the serum and reversely correlated with the expression of IFN-γ in CD4+ or CD8+ T cells in infertile patients with PCOS. These results suggested that T cell dysfunction may be involved in the pathogenesis of PCOS.

To investigate the distinctive features of lymphocytes promoting inflammation in ulcerative colitis.