Identification of TMEM178 as a Potential Prognostic Biomarker and Therapeutic Target for Breast Cancer.

Background: The transmembrane protein (TMEM) family plays important roles in cancer. However, the expression pattern and biological roles of TMEM178, a member of TMEM family, remains unclear in breast cancer (BRCA). Methods: Methylation and RNA-seq data were obtained to explore methylation level. Expression of TMEM178, methylation inhibitor 5-Aza-CdR was used to verify the effect of methylation status on the expression of TMEM178. We comprehensively investigated the prognostic outcomes, biological functions and effects on immune cell infiltration of the TMEM178 in BRCA using multiple bioinformatics methods. Results: The expression of TMEM178 was downregulated and negatively correlated with the level of DNA methylation and DNA methyltransferase (DNMT1, DNMT3A, and DNMT3B) in BRCA. Consistently, TMEM178 mRNA were confirmed to be downregulated, while upregulated in response to treatment with methylation inhibitor 5-Aza-CdR by RT-qPCR. Patients with high expression of TMEM178 have better prognosis and are more sensitive to targeted drug Pazopanib. Immune infiltration analysis showed that the infiltration levels of CD4+ T cell subsets were reduced in BRAC tissues with high TMEM178 expression, and immunosuppressive molecules of T-cell exhaustion were lower expression level. Conclusion: Hypermethylation of the TMEM178 promoter region was a contributing factor to the downregulation of its expression, and TMEM178 may reflect a prognostic and immunosuppressive situation in BRCA.

Empagliflozin modulates CD4+ T-cell differentiation via metabolic reprogramming in immune thrombocytopenia.

Immune thrombocytopenia (ITP) is an acquired autoimmune disease, in which the imbalance of CD4+ T cell subsets play a key role in the pathogenesis. Since T cells highly depend on metabolism for their function, we hypothesized that T cell dysfunction may be due to intracellular metabolic reprogramming. We found that in ITP, T cell metabolism shifts from oxidative phosphorylation to glycolysis. Empagliflozin, a sodium-glucose cotransporter 2 inhibitor, has shown regulatory metabolic effects on proximal tubular epithelial cells and cardiac cells beyond glucose lowering. However, the effects of empagliflozin on T cells remain unknown. To further investigate the metabolic dysfunction of CD4+ T cells in ITP, we explored the effect of empagliflozin on CD4+ T-cell differentiation in ITP. Our results are the first to show that increased glycolysis in CD4+ T cells resulted in an unbalanced CD4+ T-cell population. Furthermore, empagliflozin can affect the differentiation of CD4+ T-cell subsets by inhibiting Th1 and Th17 cell populations while increasing Tregs. Empagliflozin appears to regulate CD4+ T cells through inhibiting the mTOR signal pathway. Considering these results, we propose that empagliflozin could be used as a potential therapeutic option for ITP by modulating metabolic reprogramming in CD4+ T cells.

Heterogeneity of Latency Establishment in the Different Human CD4+ T Cell Subsets Stimulated with IL-15.

HIV integrates into the host genome, creating a viral reservoir of latently infected cells that persists despite effective antiretroviral treatment. CD4-positive (CD4+) T cells are the main contributors to the HIV reservoir. CD4+ T cells are a heterogeneous population, and the mechanisms of latency establishment in the different subsets, as well as their contribution to the reservoir, are still unclear. In this study, we analyzed HIV latency establishment in different CD4+ T cell subsets stimulated with interleukin 15 (IL-15), a cytokine that increases both susceptibility to infection and reactivation from latency. Using a dual-reporter virus that allows discrimination between latent and productive infection at the single-cell level, we found that IL-15-treated primary human CD4+ T naive and CD4+ T stem cell memory (TSCM) cells are less susceptible to HIV infection than CD4+ central memory (TCM), effector memory (TEM), and transitional memory (TTM) cells but are also more likely to harbor transcriptionally silent provirus. The propensity of these subsets to harbor latent provirus compared to the more differentiated memory subsets was independent of differential expression of pTEFb components. Microscopy analysis of NF-κB suggested that CD4+ T naive cells express smaller amounts of nuclear NF-κB than the other subsets, partially explaining the inefficient long terminal repeat (LTR)-driven transcription. On the other hand, CD4+ TSCM cells display similar levels of nuclear NF-κB to CD4+ TCM, CD4+ TEM, and CD4+ TTM cells, indicating the availability of transcription initiation and elongation factors is not solely responsible for the inefficient HIV gene expression in the CD4+ TSCM subset. IMPORTANCE The formation of a latent reservoir is the main barrier to HIV cure. Here, we investigated how HIV latency is established in different CD4+ T cell subsets in the presence of IL-15, a cytokine that has been shown to efficiently induce latency reversal. We observed that, even in the presence of IL-15, the less differentiated subsets display lower levels of productive HIV infection than the more differentiated subsets. These differences were not related to different expression of pTEFb, and modest differences in NF-κB were observed for CD4+ T naive cells only, implying the involvement of other mechanisms. Understanding the molecular basis of latency establishment in different CD4+ T cell subsets might be important for tailoring specific strategies to reactivate HIV transcription in all the CD4+ T subsets that compose the latent reservoir.

Altered levels of circulating CD8+CXCR5+PD-1+T follicular cytotoxic cells in primary Sjögren's syndrome.

BACKGROUND: Circulating CD8+ T-cells expressing the C-X-C chemokine receptor type 5 (CXCR5) (CD8+CXCR5+T), a recently identified follicular cytotoxic T cell subset, are involved in antiviral immunity and autoimmunity, but their abundance and role in the pathogenesis of primary Sjögren syndrome (pSS) are unknown. METHODS: Circulating CD8+CXCR5+T cell and CD8+ regulatory T cells (CD8+Treg) were evaluated in 49 pSS patients (19 patients with pulmonary involvement) and 24 age- and sex-matched healthy controls (HCs) by flow cytometry. Orthogonal partial least squares discriminant analysis (OPLS-DA) was performed, and receiver operating characteristic curves (ROC) were generated to identify characteristic cell subsets. Spearman's correlation analysis was conducted to examine the relationships between CD8+ T cell subsets and clinical features. RESULTS: The proportions and numbers of CD8+CXCR5+, CD8 + CXCR5+ programmed death 1-positive (PD-1+), and CD8+CXCR5-PD-1+T cells were significantly higher, whereas those of CD8+Treg were markedly lower, in pSS patients than HCs. The CD8+CXCR5+PD-1+T cell to CD8+Treg ratio had the greatest discriminatory power for pSS and HCs according to OPLS-DA and ROC analyses. The increased numbers of CD8+CXCR5+T cells and CD8+CXCR5+PD-1+T cells were strongly associated with those of CD4+CXCR5+T and B cells. The proportions and numbers of CD8+CXCR5+PD-1+T cells were increased in pSS patients with lung involvement. CONCLUSIONS: We identified a new CD8+CXCR5+PD-1+T subset, which was increased in abundance in pSS patients, particularly those with lung involvement, compared with HCs. Also, the CD8+CXCR5+PD-1+T to CD8+Treg ratio may be useful for identifying pSS. Our findings suggest that targeting follicular CD8+T cell subsets has therapeutic potential for pSS. Key Points • CD8+CXCR5+ T cells were expanded in the circulation of patients with pSS. • Reduced numbers CD8+Treg cells in pSS patients. • Increased CD8+CXCR5+PD-1+T cells in pSS patients with pulmonary involvement.

Traditional Thai Massage Promoted Immunity in the Elderly via Attenuation of Senescent CD4+ T Cell Subsets: A Randomized Crossover Study.

The beneficial physiological effects of traditional Thai massage (TTM) have been previously documented. However, its effect on immune status, particularly in the elderly, has not been explored. This study aimed to investigate the effects of multiple rounds of TTM on senescent CD4+ T cell subsets in the elderly. The study recruited 12 volunteers (61-75 years), with senescent CD4+ T cell subsets, who received six weekly 1-h TTM sessions or rest, using a randomized controlled crossover study with a 30-day washout period. Flow cytometry analysis of surface markers and intracellular cytokine staining was performed. TTM could attenuate the senescent CD4+ T cell subsets, especially in CD4+28null NKG2D+ T cells (n = 12; p < 0.001). The participants were allocated into two groups (low < 2.75% or high ≥ 2.75%) depending on the number of CD4+28null NKG2D+ T cells. After receiving TTM over 6 sessions, the cell population of the high group had significantly decreased (p < 0.001), but the low group had no significant changes. In conclusion, multiple rounds of TTM may promote immunity through the attenuation of aberrant CD4+ T subsets. TTM may be provided as a complementary therapy to improve the immune system in elderly populations.

γδ T Lymphocytes in Asthma: a Complicated Picture.

A minor subset (approximately 5%) of peripheral T cells has their TCR build up from γ and δ chains instead of α and ß-those are the γδ T lymphocytes. They can be functionally divided into subsets, e.g., Th1-, Th2-, Th9-, Th17-, Tfh-, and Treg-like γδ T cells. They share some specifics of both innate and adaptive immunity, and are capable of rapid response to a range of stimuli, including some viral and bacterial infections. Atopic diseases, including asthma, are one of major health-related problems of modern western societies. Asthma is one of the most common airway diseases, affecting people of all ages and having potential life-threatening consequences. In this paper, we review the current knowledge about the involvement of γδ T cells in the pathogenesis of asthma and its exacerbations. We summarize both the studies performed on human subjects as well as on the murine model of asthma. γδ T cells seem to be involved in the pathogenesis of asthma, different subsets probably perform opposite functions, e.g., symptom-exacerbating Vγ1 and symptom-suppressing Vγ4 in mice model of asthma.

IL-17 and IFN-γ Productions by CD4+ T cells and T cell Subsets Expressing NKG2D Associated with the Number of Risk Factors for Cardiovascular Diseases.

Cardiovascular diseases (CVD), which are major causes of morbidity and mortality worldwide, are characterized by complicated chronic inflammatory manifestation inducing from multi-risk factors. Previously, we have identified a pathological T cell subpopulation producing interleukin (IL)-17 in diabetes. We hypothesized that this T cell subpopulation could exist in the elderly with persistence low grade inflammation related to the risk factors for cardiovascular diseases. Thus, we investigated whether high levels of the natural group 2, member D (NKG2D) expression, IL-17 and interferon (IFN)-γ production by CD4 + T cells and T cell subsets were more prevalent in individuals who had age ≥ 60 years with > 2 risk factors for CVD (dyslipidemia, hypertension and/or diabetes mellitus) compared to subjects who had < 2 risk factors. Using flow cytometric analysis, we found that CD4 + T cells of subjects who had ≥ 2 risk factors had significantly higher NKG2D expression than those of subjects with < 2 risk factors (P = 0.023). Apparently, CD4+CD28null T subset of both two groups preferentially expressed NKG2D, and prominently produced IL-17 and IFN-γ compared to the CD4+CD28+ T subset. Expectedly, there was a statistical significance of IL-17 and IFN-γ production of CD4 + 28nullNKG2D + T cells (P = 0.037 and P = 0.042, respectively). We concluded that cumulative number of CVD risk factors associated with progressive alteration of CD4+ T cell phenotypes and their functions. Handling of metabolic risk factors may be an approach for healthcare of the elderly to prevent cardiovascular morbidity resulting from alteration of immunity.

Investigating the role of T helper related cytokines in cerebrospinal fluid for the differential diagnosis of bacterial meningitis in pre-treated paediatric patients.

Purpose: Given the challenge in the diagnosis of bacterial meningitis (BM), we assessed different cytokines in the cerebrospinal fluid (CSF) of antibiotics pre-treated patients.Materials and methods: Laboratory tests and polymerase chain reaction (PCR) were performed for 480 CSF samples from children (2 m to 14 y), suspicious to meningitis and pre-treated with antibiotics, to detect bacterial and viral aetiologies. Sixty-one CSF were included and the levels of 13 cytokines such as IL-2, IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, IL-17A, IL-17F, IL-21, IL-22, IFN-γ and TNF-α were measured using flow-cytometry.Results: All bacterial cultures were negative, but 29 and eight CSF were positive for bacterial and viral agents by PCR. IL-6, IL-10 and IFN-γ were significantly up-regulated in BM. T helper (Th) subset cytokines showed significant upregulation of Th1, Th2, Th17, Th22 and Tfh cytokines in BM. Common Th subsets cytokines (IL-6, IL-10 and TNF-α) were significantly different between the study groups. ROC curve analysis revealed good AUC for common Th related cytokines in discriminating BM.Conclusions: In pre-treated BM patients with negative bacterial cultures, cytokines IL-6, IL-10 and IFN-γ can predict BM which could be beneficial for rapid diagnosis and treatment to decrease the sequela of the disease.

Dihydroartemisinin Regulates the Th/Treg Balance by Inducing Activated CD4+ T cell Apoptosis via Heme Oxygenase-1 Induction in Mouse Models of Inflammatory Bowel Disease.

Dihydroartemisinin (DHA) is a derivative of the herb Artemisia annua L. that has prominent immunomodulatory activity; however, its underlying mechanism remains elusive. Inflammatory bowel disease (IBD) is an idiopathic inflammatory condition characterized as an autoimmune disorder that includes dysfunctions in the T helper (Th)/T regulatory cell (Treg) balance, which normally plays pivotal roles in immune homeostasis. The aim of this study was to explore the potential of DHA to ameliorate IBD by restoring the Th/Treg cell balance. To this end, we established mouse models of colitis induced by oxazolone (OXA) and 2,4,6-trinitro-benzene sulfonic acid (TNBS). We then treated mice with DHA at 4, 8, or 16 mg/kg/day. DHA treatment ameliorated colitis signs and reduced lymphocyte infiltration and tissue fibrosis. Moreover, DHA decreased the numbers of Th1 and Th17 cells and Th9 and Th22 cells in TNBS- or OXA-induced colitis, respectively, and increased Tregs in both models. DHA (0.8 mg/mL) also inhibited activated CD4+ T lymphocytes, which was accompanied by apoptosis induction. Moreover, it promoted heme oxygenase-1 (HO-1) production in vitro and in vivo, concomitant with CD4+ T cell apoptosis and restoration of the Th/Treg balance, and these effects were blocked by treatment with the HO-1 inhibitor Sn-protoporphyrin IX. Overall, these results suggest that DHA is a novel and valuable candidate for IBD therapy or Th/Treg immunoregulation.

Unraveling Natural Killer T-Cells Development.

Natural killer T-cells are a subset of innate-like T-cells with the ability to bridge innate and adaptive immunity. There is great interest in harnessing these cells to improve tumor therapy; however, greater understanding of invariant NKT (iNKT) cell biology is needed. The first step is to learn more about NKT development within the thymus. Recent studies suggest lineage separation of murine iNKT cells into iNKT1, iNKT2, and iNKT17 cells instead of shared developmental stages. This review will focus on these new studies and will discuss the evidence for lineage separation in contrast to shared developmental stages. The author will also highlight the classifications of murine iNKT cells according to identified transcription factors and cytokine production, and will discuss transcriptional and posttranscriptional regulations, and the role of mammalian target of rapamycin. Finally, the importance of these findings for human cancer therapy will be briefly discussed.

IL-10-producing regulatory B-cells suppressed effector T-cells but enhanced regulatory T-cells in chronic HBV infection.

Non-specific immune responses to antigens have been demonstrated as being enhanced during chronic hepatitis B virus (HBV) infection. Here, we evaluated the role of interleukin-10 (IL-10)-producing regulatory B-cells (Bregs) in the pathogenesis of HBV-related liver fibrosis (HBV-LF) and assessed their immunoregulatory effects. Sixty-seven patients diagnosed with chronic hepatitis B (CHB) were enrolled in this study. Numbers and frequencies of peripheral B-cells (memory CD19(+)CD24(hi)CD27(+) cells, immature/transitional CD19(+)CD24(hi)CD38(hi) cells, mature CD19(+)CD24(int)CD38(int) cells) were tested and analysed. Flow cytometry-sorted CD4(+)T cells were cultured with autologous Bregs to elucidate the effects of Bregs on CD4(+)T cells, including effector T and regulatory T-cells (Tregs). The potential immunoregulatory mechanism of Bregs was also investigated. The numbers of total B-cells and Bregs were enriched in CHB patients. The frequency of Bregs was negatively correlated with elevated alanine aminotransferase (ALT) and histological inflammation grades (G), but positively correlated with advanced histological fibrosis stages (S) and enhanced HBV replication. The phenotype of Bregs was predominantly characterized as CD19(+)CD24(hi)CD38(hi) In co-culture with Bregs, CD4(+)CD25(-)T cells from CHB patients produced less interferon-γ (IFN-γ) and IL-17 but more IL-4 than CD4(+)CD25(-)T cells alone, whereas their conversions into Tregs and IL-10(+)T cells were enhanced. In addition, Breg depletion in CHB samples dramatically decreased Treg numbers and expression of cytotoxic T-lymphocyte associated antigen-4 (CTLA-4), IL-10 and transforming growth factor-ß (TGF-ß). Moreover, the observed regulatory effect was partly dependent on IL-10 release and cell-to-cell contact. Elevated Bregs can suppress effector T but enhance Treg functions, which might influence immune tolerance in chronic HBV infection.

Telbivudine therapy may shape CD4(+) T-cell response to prevent liver fibrosis in patients with chronic hepatitis B.

BACKGROUND & AIMS: Nucleos(t)ide analogues (NAs) can indirectly restore host immunity against hepatitis B virus (HBV) by inhibiting virus replication. We aimed to investigate whether telbivudine could prevent HBV-related fibrosis progression by their influence on CD4(+) T-cell response. METHODS: Thirty-six HBeAg-positive patients with chronic hepatitis B (CHB) were enrolled for 52-week telbivudine monotherapy and were followed at treatment week (TW)-0, 4, 12, 24 and 52. By TW-52, the patients were classified into a complete-response group (CR, n = 10) with both negative HBV-DNA and HBeAg, or a part-response group (PR, n = 11) only with negative DNA, or a non-response group (NR, n = 15) still with positive DNA. The peripheral blood mononuclear cells (PBMCs) were prepared for further flow cytometric and real-time PCR analyses, and also for the in vitro experiments with primary hepatic stellate cells (HSCs). RESULTS: Peripherally, all chronic HBV-infected subjects showed the involvement of CD4(+) T-cell responses, among whom the inactive carriers (IC) had Th1 (CD4(+) IFNγ(+) ) dominated, CHB had Th17 (CD4(+) IL-17(+) ) dominated, while the immune tolerant (IT) subjects had Treg (CD4(+) CD25(high) Foxp3(+) ) dominated. Besides, we found the therapeutic responses to telbivudine were especially associated with up-regulation of Th1 and Th17, and down-regulation of Treg. Furthermore, compared to CD4(+) cells from CR, those from NR could in vitro significantly exacerbate cell activation, proliferation and cytokine production of HSCs, which were partly mediated by IL-4 and TGF-ß1. CONCLUSIONS: Telbivudine might slow down HBV-related liver fibrosis progression by restoring CD4(+) T-cell responses against HBV.

CD4+CD25high Regulatory Cells in Peripheral Blood of NSCLC Patients / 华中科技大学学报（医学）（英德文版）

The proportion and changes of CD4+CD25high regulatory T cells (Trs) in peripheral blood of non-small cell lung cancer (NSCLC) patients were analyzed and their clinical significance explored. The peripheral blood was collected from 61 patients with NSCLC and 15 healthy controls. By using monoclonal antibodies, the blood samples were evaluated with the flow cytometry for lymphocyte subsets (CD3+, CD4+ and CD8+) and CD4+CD25high Tr cells. The results showed that the proportion of CD4+CD25high Tr cells in NSCLC group was significantly higher than in control group [(4.36±2.07) % vs (2.04±1.03) %, P＜0.01]. The proportion of CD4+CD25 high Tr cells in late stage was higher than that in early stage [stages Ⅰ + Ⅱ (2.26±0.6) %; stage Ⅲ (3.28±1.38) %; stage Ⅳ(6.06±4.08) %] (P＜0.05). Kaplan-Meier survival analysis revealed that the prognosis of the patients who had higher proportion of CD4+CD25high Tr cells in peripheral blood was worse (P=0.0026). In conclusion, the relative increase in CD4+CD25high Tr cells in peripheral blood may be related to immunosuppression and tumor progression in patients with NSCLC. This finding suggests that CD4+CD25+high Tr cells in peripheral blood of NSCLC may be positive for prognosis analysis. The use of depletion of the CD4+CD25high Tr cell therapy to treat NSCLC patients may be an effective strategy.

Quantitation of T Lymphocytes and T Subsets Peripheral Blood and Cutaneous Lesion in Patients with Atopic Dermatitis / 대한피부과학회지

This study was undertaken to elucidate any quantitative abnormalities of T cells and T subsets(helper/inducer T cell: T cell and suppressor/cytotoxic. T cell; Tsc cell) in the peripheral blood and cutaneous lesion in patients with atopic dermatitis by using monoclonal antibodies, and to ascertain whether there are any relations bctwcen such immunologic abnormalities and the severity of the disease. Thirty seven patints(19 male, 18 female) were entered in this study, who vistited the Departement of Dermatology of Seoul National University Hospital frnrn February 1985 to November 1985. The control group comprised fifteen healthy children (8 male, 7 female). The peripheral blood samples of 30 patients and the skin biopsy specirnens of 29 patients were examinecl. Both were examined in 22 patients. The results showed that there was a quantitative abnormality in pcripheral blood Tsc cells in patients with atopic dermatitis and it could be related to the severity of the disease. The predominance of T cells seemed to be relatecl to the pathogenesis of atopic dematitis.

Estimation of Alteration of Peripheral Blood Immune Cells in Patients with Plopecia Areata / 대한피부과학회지

Authors have quantitated the T cell and T subsets(T and T cell) in the per- ipheral blood of 16 patients with alopecia areata and 16 normal healthy controls. The results are as follows: 1. The mean values of the T cell in total patient group(54,6+7.9g) and AAP group(5,3. 1+8. 1%) showed staticstially significant decrease when it compared with the mean value of the control group(64.6+3.6%) respectively(p<0.005). In ATU group the mean value of the T cell(53. 1+8. 1%) also showed decreasing tendency in comparison with that of control. The mean values of the T cell in total patient group(30.9+8. 9%) RIld AAP group(3'l. 5+8. %) showed statistically significant decrease when it compared with the mean value of the control group(42,6+8.9%) respectively(p<0. 005). In ATU group the mean value of the T< cell(28. 7+10. 9%) also showed decreasing tende- ncy in comparison with that of control. 3. The mean values of the Tr, cell in total patient group(6. 1+2. 2%) and AAP group(5.9+2.4%) showed staticstially significant decrease when it compared with the mean value of the control group(7.9+1.3%) respectively(p(p pl, pgp p25) In ATU group the mean value of the T cell(6. 7+0. 9%) also showed decreasing tendency in comparison with that of control. 4. The mean values of the T/T ratio showed no significant difference between the patient groups(total, AAP, ATU) and control group, respectively. Above data showed that defect of T cell and T subsets may be associated with the pathogenesis of alopecia areata.

Effects on lymphocyte & T subcytes of SARS patients treated by integrative traditional Chinese and western medicine / 中国免疫学杂志

Objective:To study the effects on lymphocyte & T subset of SARS patients treated by integrative traditional Chinese and western medicine(ICWM). Methods:48 patients were randomly divided into two groups, the control group treated by western medicine (WM) alone and the test group treated by ICWM. The test group patients took the traditional Chinese medicine by 3 weeks based on their conditions. Lymphocyte and T subset were measured. Results:① At pretreatment, absolute value of lymphocyte of 38 patients in all patients were low. There were 19 patients with lowered CD3 +, and 28 patients with lowered CD4 +/CD8 + ratio in 38 patients with T subset measured. ② The value of lymphocyte in plasma in patients after ICWM treatment increased from 1 00?10 9?0 46?10 9 L -1 to 1 92?10 9?0 74?10 9 L -1 ( P

A Study on the Quantitation of the Peripheral Blood T Lymphocytes and T Sebsets in Patients with Psoriasis by Moncolonal Antibodies / 대한피부과학회지

The study was undertaken to clarify any quantitative abnormalities in peripheral blood T lymphocytes and T subsets, mediating cell meliated immunity, and the presence of any relation between the degree of quantitative abnormalities and extent of skin lesions and activity of disease in patients with psoriasis by monoclonal antibodies. The results were as follows. 1. Mean percentages of total and suppressor T lymphocytes in 39 patients with psoriasis are significantly decreased as compared with those in 32 controls. Mean ratio of percentage of helper T lymphocytes to that of suppressor Tlymphocytes in 39 patients with psoriasis are significantly increased as compared with that in 32 controls. 2, As classified into three groups according to extent of skin lesions (E: less than 5% E,: 5-30%, and E,: more than 30%), mean pereentages of total T lymphocytes in E, and E, psoriasis group and those of suppressor T lymphocytes in all three psoriasi., groups are significantly decreased as compared with those in controIs. Mean percentages of helper T lymphor,ytes in L psoriasis group and mean ratios of percentage of helper T lymphocytes to that of suppressor T lymphocytes in E, and E, psoriasis groups are significantly increased as compared with those in controls. 3. Cis classified into three groups according to activity of disease (A,: stationary, A,: active, peripherally spreading and A,: active, small papules spreading), mean percentage of total T lymphocytes in peripheral blood lymphocytes in A, psoriasis group and those of suppressor T lymphocytes in all three psoriasis group are significantly decreased as compared with those in controls. Mean percentages of helper T lymphocytes and mean ratios of percentage if helper T lymphocytes to that of suppressor T lymphocytes in A, and A, psorixsis groups are significantly increased as compared with those in controls. These results clarified that there are quantitative abnormalities in peripheral blood I' lymphocytes and T subsets in patients with psoriasis and the degrees of abnorrnalities are related to extent of skin lesions and activity of disease. The aanorrnalities in peri.pheral blood T lymphocytes and T subsets in patients with psoriasis seem to be attributed to primary defect of suppressor T lymphoytes.

Quantitation of the Peripheral Blood T Cell and T Subsets Patients / 대한피부과학회지

The study was performed to measure and compare the peripheral blood T cell and T subsets in normal controls and psoriatic patients. Thirty-two normal controls and fift:en psoriatic patients were subjected to the study and the percentages and the rati vs of peripheral blood T cell and T subsets were measured. The results were as follows: 1. Mean percentages of peripheral blood lymphocytes reactive with OKT3 monoclonal antibody in psoriatic patients were 72. 8+-8. 2%, They decreased significantl) as compared with these in control group(76, 6- i-4. 7%). Mc an percentages of peripheral blood lymphocytes reactive with OKT4 monoclonal antibody in psoriatic patients were 47. 3+6, 7p;. They increased as compared with these in control group(46. 5+-3. 9p;), but the increase was insignificant. 3. Mean percentages of peripheral blood lymphocytes reactive with OKT8 monoclonal antibody in psoriatic patients were 27. 2+5. 5g, They decreased significantly as compared with these in control group(30, 6- l-4. 3%) 4. Mean ratios of lymphocytes reactive with OKT4 monoclonal antibody to these reactive with OKT8 monoclonal antibody in psoriatic patients were 1.8+- 0. 48 They increased significantly as compared with these in control group(1. 6+ 0.34).

T Subsets and Antitumor Activity of Lymphocytes Infiltrating Hunan Primary Brain Gliomas / 第二军医大学学报

Glioma-infiltrating lymphocytes (GIL) were isolated from 9 surgical biopsy specimens of primary brain gliomas using mechanical and enzymatic digestion and discontinuous density gtadient centrifugation. During cultured in the presence of interieukin-2 (IL-2) for a period of four weeks, GIL were expanded 48.4-fold on the averags, even up to 118-fold. GIL activated by IL-2 had specific cytorytic activity against autologous glioma cells. Analysis of T subsets of GIL freshly isolated showed that CD3+ cells were 71.0?11.9%, CD4+ cells 34.2?6.1% and CD8+ cells 37.0?7.6%. Ability of activated GIL to secrete ?-interferon (?-IFN) was significantly higher than that of freshly isolated GIL and autologous peripheral blood lymphocytes (PBL). The results suggest that GIL have many advantages for an adoptive immunotherapy of patients with brain gliomas and is a new type of antitumor immune effector.