Circulating CD2 Negative T Cells in Pediatric Acute Leukemia

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5151-5151
Author(s):  
Weijie Li ◽  
Lei Shao ◽  
Atif Ahmed ◽  
Doug Myers ◽  
Keith J August

Abstract Introduction: Leukemia cells are able to escape from immunosurveillance using immune tolerance mechanisms as the majority of leukemia antigens are either shared or aberrantly expressed self-proteins. T cells reactive to these antigens are purged during thymic selection. CD2, a pan-T-cell antigen, is expressed early during T cell developments in thymus and is found on all subsets of mature T cells. Recent studies show that there are low levels of extrathymic CD2 negative (CD2-) T cells, which show immature T cell features and can be induced to differentiate into mature helper and cytotoxic T cells in vitro. Since circulating CD2- T cells could represent pre-selection immature T cells, they may play an important role in tumor immunity. Methods: 81 pediatric B-cell acute lymphoblastic leukemia (B-ALL) patients, 22 pediatric acute myeloid leukemia (AML) patients and 22 normal controls were included in this study. B-ALL group included 45 NCI-standard risk (SR) patients and 36 NCI-high risk patients. All the leukemia patients were diagnosed at Children's Mercy Hospital in the past ten years with a diagnostic peripheral blood (PB) specimen. The PB specimens were studied by four-color multiparameter flow cytometry with antibodies for T cell markers (CD2, CD3, CD4, CD5, CD7 and CD8) and CD45, and analyzed by BD FACSDiva 8.0.1. CD2- and CD3+ T cells were recorded as % of total T cells. Student's t-test was used to compare results. Results: The percentages of CD2- T cells in AML (mean ± STD: 1.31% ± 1.41%) and B-ALL (0.84% ± 0.67%) were significantly higher than that seen in control group (0.51% ± 0.52%, p<0.05). No significant difference was found between AML and B-ALL. There was no significant difference between HR B-ALL (0.96% ± 0.81%) and SR B-ALL (0.74% ± 0.52%). Interestingly, CD2- T cells in 4/5 B-ALLs with 11q23 (KMT2A) rearrangement were undetectable. All 3 therapy-related AML patients studied had KMT2A gene rearrangement, and had no detectable CD2- T cells with poor clinical outcome (overall survival less than 1 year). The 3 AMLs associated with Down syndrome, a prognostically favorable AML group, showed relative high levels (≥ 1.49%) of CD2- T cells. Conclusions: Circulating CD2- T cells are increased in peripheral blood in pediatric AML and B-ALL patients. KMT2A gene rearrangement, an unfavorable cytogenetic abnormality, is associated with a decrease in CD2- T cells. The relationship of KMT2A gene rearrangement and decrease in circulating CD2- T-cells as well as the relationship of CD2- T cells to clinical outcome should be evaluated in future studies. The role of CD2- T cells in tumor specific immunomodulation should be explored, and may impact future studies of cell-based cancer immunotherapeutics. Disclosures No relevant conflicts of interest to declare.

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5603-5603 ◽  
Author(s):  
Cherie Tracy Ng ◽  
Jeanette Ampudia ◽  
Robert J. Soiffer ◽  
Jerome Ritz ◽  
Stephen Connelly

Background: CD6 is a co-stimulatory receptor, predominantly expressed on T cells, that binds to activated leukocyte cell adhesion molecule (ALCAM), a ligand expressed on antigen presentation cells and various epithelial and endothelial tissues. The CD6-ALCAM pathway plays an integral role in modulating T cell activation, proliferation, differentiation and trafficking and is central to inflammation. While effector T cell (Teff) are CD6hi and upregulate expression upon activation, regulatory T cells (Treg) remain CD6lo/-, making this an attractive target to modulate Teff activity while preserving Treg activity. Early studies by Soiffer and colleagues demonstrated using T12, an anti-CD6 monoclonal antibody (mAb) that ex-vivo depletion of CD6+ donor cells prior to transplantation decreased the incidence of both acute and chronic GVHD, highlighting the importance of CD6+ cells in GVHD pathogenesis and validating it as a therapeutic target. However, it remains to be shown whether modulating the CD6-ALCAM pathway in vivo can attenuate GVHD. We investigated the use of itolizumab, a humanized anti-CD6 mAb that has demonstrated clinical efficacy in other autoimmune diseases, as both a preventive and therapeutic treatment for GVHD, using a humanized xenograft mouse model. Methods: Humanized xenograft mice were generated by intravenous transfer of 2x10^7 human PBMCs into 6-8 weeks old NOD/SCID IL2rγ-null (NSG). To investigate the ability of itolizumab to prevent GVHD, mice were dosed with either 60μg or 300μg of itolizumab, 150μg of abatacept (CTLA4-Ig), or vehicle, starting one day prior to PBMC transplantation. To investigate the therapeutic effect of itolizumab, mice were dosed with either 150μg of itolizumab or vehicle, starting at Day 5 post-PBMC transfer, when transplanted T cells are already activated. All treatments were administered IP every other day. Weight and disease scores were monitored throughout the study. At Days 18 and 35, peripheral blood was evaluated by flow cytometry to examine T cell prevalence, and tissues were collected for histological examination of pathology and T cell infiltration. Results: When administered as prevention (Day -1), treatment with either 60μg or 300μg of itolizumab significantly decreased mortality compared to the vehicle control (100% vs. 10%); this decrease was similar to the positive control group treated with abatacept (Figure 1). At 60μg, itolizumab-treated mice demonstrated significant reductions in the prevalence of human T cells in peripheral blood vs. vehicle-treated mice at Day 18 (<0.2% vs. 74.5%; p < 0.001). The reduction in peripheral T cells was accompanied by reductions in tissue-infiltrating T cells in lung (85-fold) and gut (9.5-fold), as well as reductions in disease scores and weight loss. When administered therapeutically, treatment with itolizumab was associated with a survival rate of 50% compared to 10% in the control group (Figure 2). Similarly, peripheral T cell prevalence (34.3% vs. 65.1%; p < 0.001), weight loss, and disease scores were inhibited by itolizumab compared to vehicle control mice. Conclusions: These data suggest that systemic treatment with itolizumab can modulate pathogenic Teff cell activity, establishing this antibody as a potential therapeutic for patents with GvHD. A phase I/II study using itolizumab as first line treatment in combination with steroids for patients with aGVHD is currently ongoing (NCT03763318). Disclosures Ng: Equillium: Employment, Equity Ownership. Ampudia:Equillium: Employment. Soiffer:Mana therapeutic: Consultancy; Kiadis: Other: supervisory board; Gilead, Mana therapeutic, Cugene, Jazz: Consultancy; Juno, kiadis: Membership on an entity's Board of Directors or advisory committees, Other: DSMB; Cugene: Consultancy; Jazz: Consultancy. Ritz:Equillium: Research Funding; Merck: Research Funding; Avrobio: Consultancy; TScan Therapeutics: Consultancy; Talaris Therapeutics: Consultancy; Draper Labs: Consultancy; LifeVault Bio: Consultancy; Celgene: Consultancy; Aleta Biotherapeutics: Consultancy; Kite Pharma: Research Funding. Connelly:Equillium: Employment, Equity Ownership.


2015 ◽  
Vol 52 (1) ◽  
pp. 55-58 ◽  
Author(s):  
Sedat IŞIKAY ◽  
Nurgül IŞIKAY ◽  
Halil KOCAMAZ

Background Familial Mediterranean Fever and celiac disease are both related to auto-inflammation and/or auto-immunity and they share some common clinical features such as abdominal pain, diarrhea, bloating and flatulence. Objectives We aimed to determine the association of these two diseases, if present. Methods Totally 112 patients diagnosed with Familial Mediterranean Fever and 32 cases as healthy control were included in the study. All participants were examined for the evidence of celiac disease, with serum tissue transglutaminase IgA levels (tTG IgA). Results Totally 144 cases, 112 with Familial Mediterranean Fever and 32 healthy control cases were included in the study. tTG IgA positivity was determined in three cases with Familial Mediterranean Fever and in one case in control group. In that aspect there was no significant difference regarding the tTG IgA positivity between groups (P=0.81). Duodenum biopsy was performed to the tTG IgA positive cases and revealed Marsh Type 3b in two Familial Mediterranean Fever cases and Marsh Type 3c in the other one while the biopsy results were of the only tTG IgA positive case in control group was Marsh Type 3b. In HLA evaluation of the celiac cases; HLA DQ2 was present in two celiac cases of the Familial Mediterranean Fever group and in the only celiac case of the control group while HLA DQ8 was present in one celiac case of the Familial Mediterranean Fever group. Conclusions We did not determine an association of Familial Mediterranean Fever with celiac disease. Larger studies with subgroup analysis are warranted to determine the relationship of these two diseases.


Author(s):  
Erdal Kurnaz ◽  
Yaşar Şen ◽  
Süleyman Aydın

AbstractBackground:The aim of this study was to determine the serum levels of kisspeptin and ghrelin (GAH), as well as the relationship of these two peptides with each other in premature thelarche (PT) and premature adrenarche (PA) cases and to investigate the possibility of using these peptides as markers in the differentiation of puberty disorders.Methods:A PT group aged 1–8 years (n = 40), a PA group aged 1–9 years (n = 23, female/male = 20/3) and control groups consistent with each of the previous groups in terms of age and gender were created for the study. Kisspeptin and ghrelin levels were measured with ELISA methods from blood samples drawn while fasting in the morning.Results:When the PT group was compared with the controls, the plasma kisspeptin levels of the cases were significantly higher than the control group (165.47 ± 15.45 pmol/L, 96.82 ± 12.33 pmol/L, p = 0.005, respectively). Kisspeptin levels in the PA group did not show a difference with the control group (121.36 ± 17.99 pmol/L, 95.52 ± 11.54 pmol/L, p = 0.249, respectively). No significant difference could be found when GAH levels in the PT and PA groups were compared with controls. No significant correlation was found between kisspeptin and GAH levels in the PT and PA groups.Conclusions:Our results indicate that kisspeptin plays an important role in the PT, but GAH is not associated with puberty disorders.


2019 ◽  
Vol 9 (6) ◽  
pp. 865-869
Author(s):  
Xuecheng Zhang ◽  
Ning Su ◽  
Dong Chen

Immunoglobulin A nephropathy (IgAN) is a primary glomerulonephritis characterized by abnormal immune response-mediated deposition of polymeric IgA (pIgA) in mesangium. As a type of important immune cells, the relationship of CD3 or CD4 with the pathogenesis of IgAN remains poorly understood. In this study, 38 patients with IgAN, 7 patients with idiopathic membranous nephropathy (MN) and 46 healthy adults without history of kidney disease were enrolled. Peripheral blood was collected for further evaluation of the expressions of CD3 and CD4 and IgA by flow cytometry, quantitative polymerase chain reaction (qPCR) and Western blot. Meanwhile, the expression of IgA was detected by ELISA. The result showed that expression of CD3 T cells was down-regulated in patients with IgAN, while amounts of CD4 T cells and IgA level were significantly increased compared to normal control (P < 0.05). However, no signficant changes in CD3, CD4 T cells were found in patients with MN. Our study demonstrates that CD3 and CD4 T cells as well as IgA are involved in the pathogenesis of IgAN and these targets might be beneficial for the treatment of IgAN.


Open Medicine ◽  
2010 ◽  
Vol 5 (4) ◽  
pp. 431-436
Author(s):  
Bülent Karagöz ◽  
Oğuz Bilgi ◽  
Emin Kandemir ◽  
Alev Erikçi ◽  
Özkan Sayan ◽  
...  

AbstractTo investigate CD4+CRTH2+ cells in peripheral blood in advanced stage non small cell lung cancer (NSCLC) patients. Forty-six patients with advanced stage NSCLC, who are chemotherapy or radiotherapy naïve, and 17 healthy volunteers, were enrolled in this study. The study was performed using flow cytometry and a complete blood cell counter analyser. CD4+ T cell percentage, CD4/CD8 ratio, CRTH2+CD4+ cell percentages, counts, and mean fluorescein intensity (MFI) and hematological parameters were evaluated in both groups. A survival analysis was performed to compare the patients with high CD4+CRTH2+ cell percentage and those with low CD4+CRTH2+ percentage. CD4+ T cell percentage in total lymphocytes and the CD4/CD8 ratio were lower in the patient group than in the control group. The absolute CD8 T cell count was higher in the patient group than in the control group, whereas the total T cells was not different. The CRTH2+ cell percentage in CD4+ T cells (7.96% ± 6.21% vs 3.37% ± 3.55%; respectively; p: 0,001) and the absolute count of CRTH2+CD4+ cells ( 97 mm-3 ± 109 mm-3 vs 37 mm-3 ± 38 mm-3, respectively; p: 0,033) in the patient group were higher than in the control group, but CRTH2-PE MFI values were not different between groups. Cox regression analysis did not show that CRTH2+CD4+ cell count or percentage is an independent prognostic factor. The study found that CRTH2 expression of CD4+ T cells and CRTH2+CD4+ cell number are higher in the peripheral blood of NSCLC patients than in that of healthy subjects. Further studies that explore the biological significance of high CD4+CRTH2+ cells in lung cancer patients, should be pursued.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3753-3753
Author(s):  
Zonghong Shao ◽  
Meifeng Tu ◽  
Hong Liu ◽  
Guangsheng He ◽  
Jun Shi ◽  
...  

Abstract Objective To detect the quantities of monocyte-derived dendritic cell precursors (pDC1) and plasmacytoid dendritic cell precursors (pDC2) in peripheral blood mononuclear cells (PBMC) of severe aplastic anemia (SAA) patients before and after immune suppressive therapy (IST), the ratio of their pDC1 to pDC2, and the expression of T-cell co-stimulating molecules (CD80, CD86, CD40) on dentritic cells (DC) and B cells surface in the SAA patients’ peripheral blood. Methods with three-color monoclonal antibody labeling technology, the quantities and ratio of pDC1 and pDC2 in PBMC were detected in 26 patients with SAA at active phase,13 patients with SAA at recovery phase and 15 normal control respectively by FACS. The aforementioned merits of 10 SAA patients were tested before and 2 months after IST by FACS. By FACS, the expression of CD80, CD86 and CD40 on DC and B lymphocytes were detected in 16 patients with SAA and 15 normal controls. Results The percentages of total pDC, pDC1, pDC2 and the ratio of pDC1/pDC2 of controls (healthy people) were(0.72±0.32)%,(0.41±0.18)%,(0.30±0.21)%, 1.58±0.69 respectively, and those of the patients with SAA at active phase were(0.96±0.92)%,(0.67±0.65)%,(0.32±0.30)%,2.70±1.63 respectively. The differences were significant [pDC1 (P<0.05); pDC1/pDC2 ratio (P<0.01)]. The aforementioned merits of recuperating SAA patients decreased to (0.77±0.48)%,(0.43±0.37)%,(0.34±0.34)%,1.78±1.29 respectively, which were not significantly different from those of normal control group. The aforementioned merits of 10 SAA patients were(0.87±0.98)%,(0.35±0.30)%,2.65±1.27 before IST, and(0.24±0.28)%,(0.14±0.14)%,2.16±0.82 after IST, with significant decreases of pDC1 and pDC2 (P<0.05). The percentages of CD80, CD86 and CD40 expression on DC in peripheral blood of healthy control were(1.61±2.37)%,(11.97±12.18)%,(0.56±1.26)% respectively, and those of SAA patients were(9.14±12.89)%,(29.84±9.56)%,(7.04±11.99)% respectively. There was a significant difference of CD86 expression (p<0.05) between SAA patient and normal control groups. The percentages of CD19, CD80, CD86 and CD40 expression on lymphocytes in peripheral blood of healthy control group were (9.38±3.18)%,(2.57±1.51)%,(1.86±1.11)%,(7.34±4.21)% respectively, and those of SAA patients were(11.12±9.02)%,(5.17±2.72)%,(5.98±3.84)%,(8.85±9.95)% respectively. There were significant differences of CD80 and CD86 expressions (P<0.05, P<0.01) between SAA and control groups. The percentages of CD80, CD86 and CD40 expression on B lymphocytes of control were(28.22±12.32)%, 8.04±2.27% and(81.6±22.45)% respectively, and those of SAA patients were(23.06±14.9)%,(20.46±11.1)%,(81.57±21.14)% respectively. There was a significant difference of CD86 expression (p<0.05) between patient and control groups. Conclusion The pDC subtypes were abnormal and the percentage of pDC1 increased in SAA patients, which were associated with the state of this illness. DC and B Lymphocytes in SAA up-regulated the expression of T cell co-stimulating molecules (CD86) that draw the T lymphocyte abnormally activated.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 600-600
Author(s):  
Christopher C. Porter ◽  
Mark A. Gregory ◽  
Vadym Zaberezhnyy ◽  
Jelena Klawitter ◽  
Uwe Christians ◽  
...  

Abstract Abstract 600 Although therapy for Bcr-Abl+ leukemia has been revolutionized by the development of the tyrosine kinase inhibitors (TKI), some patients, particularly those with advanced phase chronic myeloid leukemia or acute lymphoblastic leukemia (ALL) have unsatisfactory responses. We have demonstrated that inhibition of calcineurin with cyclosporine (CsA) increases the sensitivity of Bcr-Abl cells to TKI; furthermore, combination therapy with CsA plus dasatinib cured all mice with Bcr-Abl+ ALL, whereas all of the mice treated with dasatinib alone died with leukemia (Gregory et al, Cancer Cell, 2010). While the synergistic effect is independent of MDR1 inhibition by CsA in vitro, the possibility remains that the demonstrated survival advantage of combination therapy is due to altered pharmacokinetics (PK)and increased dasatinib exposure. We sought to determine if co-administration of CsA with dasatinib alters dasatinib PK, if differences in PK are sufficient to explain differences in response to therapy in vivo, and if combination therapy appears to adversely affect T-cell numbers. Bl6 mice were treated with dasatinib (20mg/kg/d), cyclosporine (25mg/kg/d), or both by oral gavage. Serum from peripheral blood was obtained at 0, 1, 2, 4, 8, 12, 24, and 48 hours after single doses and after one week of therapy (trough, 1, 2, 4, 8, and 12 hours). Dasatinib levels were determined by LC/LC-MS/MS. Pharmacokinetic (PK) analyses indicate that after 1 week of therapy, co-administration of CsA with dasatinib increases the Cmax and AUCinf of dasatinib as compared to dasatinib alone (277.4 v. 107.7 ng/ml and 916.8 v 487.4 ng/ml*hr, respectively; Figure A). The PK profiles suggest that co-administration of CsA with dasatinib enhances enteric absorption of dasatinib, but has little effect on its systemic elimination. Next, Arf-/-Bcr-Abl+GFP+ leukemia cells (Williams et al, Genes Dev, 2007) were transferred into unirradiated recipients which were treated with dasatinib (10 or 20 mg/kg/d) or with combination therapy (CsA 25mg/kg/d with dasatinib 5 or 10 mg/kg/d) for 7 days. Leukemia bearing mice were euthanized and the bone marrow (BM), peripheral blood (PBL) and spleens (SPL) were assessed for leukemia burden by flow cytometry. Combined CsA and dasatinib results in better disease control, even at doses predicted to result in similar exposure to dasatinib alone (i.e. half). For example, the mean percentage of GFP+B220+ BM cells was 6.7% in mice treated with dasatinib 10mg/kg/d as compared to 0.1% in mice treated with dasatinib 5mg/kg/d plus CsA (p<0.05; ANOVA/Bonferroni; Figure B). These data suggest that the synergistic effects of combining calcineurin inhibition and TKI are not due to altered PK alone. Since CsA is an immunosuppressant and there is data to suggest an immunosuppressive effect of dasatinib (Schade et al, Blood, 2008), we also measured the percentages of T-cells in the PBL and SPL of mice treated with dasatinib or CsA plus dasatinib. In this short-term experiment, there was little effect of combined therapy on the percentages of PBL and SPL T-cells as compared to dasatinib alone. For example, there was no significant difference in the percentage of CD3+B220neg cells in the PBL among the 4 groups of treated mice (p=NS; ANOVA; Figure C). Ongoing studies are designed to define the PK of dasatinib at the lower doses when combined with CsA, the effect of combined therapy on T-cell function, and long-term outcomes in mice with Bcr-Abl+ leukemia treated with CsA and lower doses of dasatinib as compared to dasatinib alone. These data support the development of early phase studies of combined therapy for Bcr-Abl+ leukemia. Disclosures: Off Label Use: The use of cyclosporine as adjunctive therapy for Bcr-Abl+ leukemia will be suggested.


2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Guohua Li ◽  
Sheng Zeng ◽  
Wangdi Liao ◽  
Nonghua Lv

Objective. To study effect and its mechanism of Bifid Triple Viable for initially treating ulcerative colitis with 5-aminosalicylic acid.Methods. 82 patients, who were firstly diagnosed as ulcerative colitis, were randomized into experiment group (41 cases, treated with Bifid Triple Viable and Etiasa) and control group (41 cases, treated with Etiasa). The clinic symptom score, colon mucosa inflammation score, and some immune indices were detected and compared between two groups before and two months after treatment.Results. Two months after treatment, the clinical symptom score, colon mucosa inflammation score, and IL-1βexpression in colon mucosa decreased significantly (P<0.01), and IL-10 and IgA expressions in colon mucosa increased significantly (P<0.01). Those differences were more marked in experiment group than control group (P<0.05). However, peripheral blood T cell subgroup, immunoglobulins, and complements had no significant difference between two groups two months after treatment, but the ratio of peripheral blood CD4+ T cell to CD8+ T cell in experiment group increased more than that in control group (P<0.05).Conclusion. Bifid Triple Viable contributed to Etiasa to treat ulcerative colitis in inducing remission period, which was perhaps related to affecting the patient’s immune function.


Author(s):  
Juan Li ◽  
Xiao-fei Sun ◽  
Ying Shen ◽  
Qing Yang ◽  
Shu-yan Dai

<b><i>Objective:</i></b> To investigate the expression of T-cell immunoglobulin and mucin domain 3 (TIM-3) on peripheral T cells of cervical carcinoma patients. <b><i>Methods:</i></b> Peripheral blood samples from 15 high-grade cervical squamous intraepithelial lesion (HSIL) patients, 24 cervical carcinoma patients, and 21 healthy controls were collected. TIM-3 expressions on the surface of peripheral CD4+ T cells and CD8+ T cells were analyzed with flow cytometry. <b><i>Results:</i></b> There was significantly lower expression of CD4+ T cells and CD8+ T cells in HSIL patients and cervical carcinoma patients compared with healthy controls. We also found that TIM-3 expression on peripheral CD4+ T and CD8+ T cells of both HSIL patients and cervical carcinoma patients was significantly increased compared to the control group. Further analyses revealed that the expression of TIM-3 on peripheral CD4+ T and CD8+ T cells significantly increased in stage III–IV cervical carcinoma patients compared to stages I–II. <b><i>Conclusion:</i></b> The increased expression of TIM-3 on CD4+ T cells and CD8+ T cells of patients with cervical carcinoma and HSIL suggests the potential role of TIM-3 in the development and progression of cervical carcinoma, which may be a novel therapy target for cervical carcinoma.


2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Nange Zhao ◽  
Tingting Zhang ◽  
Yujuan Zhao ◽  
Jianping Zhang ◽  
Keqiang Wang

Objective. To investigate the quantity of CD4+T, CD4+T, CD8+T, and γδT cells in peripheral blood of HIV-infected/AIDS patients as well as to explore the possible role of CD4/CD8 ratio and γδT cells in the progression of HIV/AIDS, aimed at providing evidence for the diagnosis and treatment of AIDS. Methods. The quantity levels of CD3+T cells, CD4+T cells, CD8+T cells, and γδT cells in peripheral blood of 46 HIV-infected/AIDS patients and 30 healthy controls were detected by using flow cytometry. Results. The count of CD3+T, CD4+T, CD8+T, and γδT cells ( x ¯ ± s , A/μl) in the peripheral blood was 1183.64 ± 132.58 , 278.39 ± 122.38 , 863.13 ± 82.38 , and 22.53 ± 1.74 in the experimental group as well as 1456.46 ± 124.37 , 788.74 ± 189.67 , 569.61 ± 46.49 , and 10.96 ± 0.28 in the control group, respectively. The p values of the two groups were <0.005 after the t -test, revealing a statistically significant difference. The proportion of CD3+T, CD4+T, CD8+T, and γδT cells in total lymphocytes in the two groups ( x ¯ ± s , %) was 71.83 ± 5.37 , 13.39 ± 2.23 , 62.93 ± 5.81 , and 3.67 ± 0.87 in the experimental group, respectively. In the control group, the values were expressed as 66.72 ± 5.48 , 42.77 ± 3.38 , 31.41 ± 3.62 , and 1.73 ± 0.36 , respectively. After performing the t -test, p values in the two groups were <0.005 except CD3+T, with statistically significant differences. Besides, CD4/CD8 was 0.33 ± 0.11 in the experimental group and 1.48 ± 0.29 in the control group, t = 26.528 , p < 0.001 , exhibiting a significant statistical difference. Conclusion. HIV infection induces the activation and proliferation of CD8+T and γδT cells, contributing to the decrease of CD4+T cells, while CD8+T and γδT cells are involved in the immune response and tissue damage after HIV infection.


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