Relevant bibliographies by topics / Lymphocytes T CD8 intratumoraux

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Academic literature on the topic 'Lymphocytes T CD8 intratumoraux'

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Published: 1 February 2025

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Journal articles on the topic "Lymphocytes T CD8 intratumoraux"

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Dimitrova, Polina D., Savelina L. Popovska, and Ivan N. Ivanov. "A Study on Tumor-Infiltrating Lymphocytes in Different Subtypes of Breast Cancer." Journal of Biomedical and Clinical Research 14, no. 1 (June 1, 2021): 70–81. http://dx.doi.org/10.2478/jbcr-2021-0008.

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Summary The study aimed to investigate immune cell infiltration in different subtypes of breast cancer (BC). Retrospectively were selected 100 patients with primary BC, grouped into four molecular surrogate subtypes (Luminal A and Luminal B-like, HER2-positive and triple-negative - TN), determined by immunohistochemistry (IHC). In each patient, a percentage of stromal tumor-infiltrating lymphocytes (TILs) was determined by hematoxylin-eosin staining. IHC was performed using primary antibodies CD3, CD4, CD8, CD20, and FOXP3. Immunophenotyped lymphocytes were counted (separately intratumoral and stromal) and semi-quantitatively graded. In the studied tumors, 10% were defined as lymphocyte-predominant BC. A high count of intratumoral and stromal TILs subsets was found mainly in TN and HER2-positive BC. The stroma is the preferred localization for immune cells in all four BC subtypes. CD3+ T predominates over CD20+ B lymphocytes, with CD8+ T cytotoxic and FoxP3+ T regulatory cells dominating T subtypes. HER2 and TN are more immunogenic than Luminal A and Luminal B – like subtypes of BC. The T-cells’ immune response was predominant in the studied cases of BC, with a predominance of CD8+ Tc and Foxp3+ Treg cells located mainly in the stroma.
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Pyo, Jung-Soo, Byoung Kwan Son, Hyo Young Lee, Il Hwan Oh, and Kwang Hyun Chung. "Prognostic Implications of Intratumoral and Peritumoral Infiltrating Lymphocytes in Pancreatic Ductal Adenocarcinoma." Current Oncology 28, no. 6 (November 1, 2021): 4367–76. http://dx.doi.org/10.3390/curroncol28060371.

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This study aimed to elucidate the prognostic implications of intratumoral and peritumoral infiltrating T-lymphocytes in pancreatic ductal adenocarcinoma (PDAC) through a meta-analysis. A total of 18 eligible studies and 2453 PDAC patients were included in the present study. Intratumoral and peritumoral infiltrating lymphocytes were evaluated using various markers, such as CD3, CD4, CD8, FOXP3, and immune cell score. The correlations between these parameters and overall and disease-free survival were investigated and used in the meta-analysis. High intratumoral infiltration of CD3-, CD4-, and CD8-expressing lymphocytes was significantly correlated with better overall survival (hazard ratio (HR) 0.747, 95% confidence interval (CI) 0.620–0.900, HR 0.755, 95% CI 0.632–0.902, and HR 0.754, 95% CI 0.611–0.930, respectively). However, there was no significant correlation between PDAC prognosis and intratumoral FOXP3 or immune cell score (HR 1.358, 95% CI 1.115–1.655 and HR 0.776, 95% CI 0.566–1.065, respectively). Moreover, there was no significant correlation between the prognosis and peritumoral infiltrating T-lymphocytes. In evaluations of disease-free survival, only high intratumoral CD4 infiltration was correlated with a better prognosis (HR 0.525, 95% CI 0.341–0.810). Our results showed that high intratumoral infiltrating lymphocytes were significantly correlated with a better PDAC prognosis. However, among the tumor-infiltrating lymphocytes, CD3, CD4, and CD8 had prognostic implications, but not FOXP3 and immune cell score.
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Adashek, Michael, Abigail Sy Chan, Johnathan Heath, Rachel Fanaroff, Michael E. Kallen, Joseph S. Friedberg, Melissa Culligan, Tamara Khashab, and Kenneth David Miller. "Prognostic value of tumor infiltrating lymphocytes in epithelioid malignant pleural mesothelioma." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e20064-e20064. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e20064.

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e20064 Background: Malignant Mesothelioma (MM) is an aggressive malignancy with survival of 4-12 mo. without treatment and 10% 5-year survival. The response of patients with MM to immunotherapy has increased interest in the tumor immune microenvironment. The purpose of this study was to determine if tumor infiltrating lymphocytes (TIL) are correlated with survival in epithelioid MM. Methods: Immunohistochemistry was performed on specimens from 27 patients with epithelioid mesothelioma using CD4, CD8, and CD68 antibodies. Infiltrate density was scored (0-3+) by pathologist estimate in intratumoral and adjacent tumoral tissue. ANOVA and regression analysis were performed. Overall survival (OS) for the entire group and time to progression (TTP) for nine patients with known time from surgery until tumor recurrence were also studied as a surgical resection subgroup (SRG). Results: For the small SRG the relationship between (TTP) and TIL score of CD8 at the edge of the tumor was significant (F[2,6]=5.64, P=.042) however TIL score of intratumoral CD8 cell infiltrates and TTP did not demonstrate statistical significance. The relationship between OS with CD8 infiltrate at the tumor edge, for the entire group, approached significance at (F [3,22]=2.93, P=0.056). TTP and OS and the TIL score of CD4, CD68 at both tumor center and tumor edge did not demonstrate statistical significance. Conclusions: CD8+ lymphocytes are an important component of host immune defense against cancer. We found that in epithelioid MM the cellular infiltrate of CD8 lymphocytes at the edge of the tumor (but not with intratumoral CD8) was associated with longer time to recurrence. TTP and OS were not associated with CD4 and CD68 within or at the tumor edge. The role of CD8 T-cells and the quantitative difference between CD8 at the edge of tumor and intratumoral CD8 should be further investigated in order to optimize immunotherapy.
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O'Callaghan, D., E. Rexhepaj, K. Gately, W. M. Gallagher, D. Delaney, E. Kay, and K. O'Byrne. "Effect of pattern of lymphocyte infiltration in NSCLC on outcome." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 11079. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.11079.

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11079 Background: The role played by the immune system in determining survival in non-small-cell lung cancer (NSCLC) is unclear. The aim of this study was to investigate the prognostic significance of T-lymphocyte infiltration in NSCLC focusing on CD3+, cytotoxic CD8+ and FOXP3+ T regulatory (Treg) cells. Methods: Immunohistochemistry was used to detect CD3+, CD8+ and FOXP3+ lymphocytes in the tumor islets and tumor stroma in 186 patients with surgically resected NSCLC with a minimum follow-up of 3 years. Quantification of immune infiltration was performed using the Aperio automated image analysis system incorporating the Genie software tool. The median of tumor:stroma CD3+, CD8+ and FOXP3+ infiltration ratios were used as thresholds to dichotomise patients to either high or low infiltration rates. Prognostic variables were identified using univariate and Cox multivariate analysis. Kaplan-Meier analysis and the log-rank test were used to illustrate differences in overall survival. Results: Patients with a higher intratumoral CD3+ and CD8+ lymphocyte infiltration ratio had significantly better survival compared to those with a low tumour/stroma infiltration ratio (p=0.023 & <0.001 respectively). Conversely high intratumoral T-regulatory FOXP3+ positive lymphocyte infiltration rates were associated with a particularly poor prognosis independent of surgical stage (p<0.001). Conclusions: Microlocalization of infiltrating T-lymphocytes, in particular Treg cells, is a powerful predictor of outcome for surgically resected NSCLC and compares favourably with recently published prognostic genomic approaches. Assessment of inflammatory cell infiltrates may help determine which patients should receive adjuvant chemotherapy and, in the future, in predicting benefit from novel adjuvant vaccine/immunotherapies. No significant financial relationships to disclose.
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Asioli, Sofia, Lidia Gatto, Uri Vardy, Claudio Agostinelli, Vincenzo Di Nunno, Simona Righi, Alicia Tosoni, et al. "Immunophenotypic Profile of Adult Glioblastoma IDH-Wildtype Microenvironment: A Cohort Study." Cancers 16, no. 22 (November 18, 2024): 3859. http://dx.doi.org/10.3390/cancers16223859.

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Background: Glioblastoma IDH-wildtype (GBM IDH-wt) is the most aggressive brain tumor in adults and is characterized by an immunosuppressive microenvironment. Different factors shaping its tumor microenvironment (TME) regulate tumor progression and treatment response. The aim of this study was to characterize the main immunosuppressive elements of the GBM IDH-wt TME. Methods: Immunohistochemistry for CD3, CD4, CD8, CD163, programmed death ligand 1 (PD-L1) and programmed death 1 (PD1) was performed on surgical tumor specimens from patients diagnosed with GBM IDH-wt, according to the CNS WHO 2021 criteria. The impact of categorical variables on time-dependent outcomes such as overall survival (OS) and progression-free survival (PFS) has been estimated through the Kaplan–Meier method. Results: We included 30 patients (19 males and 11 females), median age of 59.8 years (range 40.2–69.1 years). All patients underwent surgery followed by temozolomide concurrent with and adjuvant to radiotherapy. MGMT was methylated in 14 patients (47%) and unmethylated in 16 patients (53%). The overall absolute percentages of CD4+ lymphocytes, both intratumoral and perivascular, were significantly more represented than CD8+ lymphocytes in the TME (p = 0.02). A low density of CD4+ lymphocytes (≤10%) was found to be a favorable prognostic factor for GBM outcome (p = 0.02). Patients with MGMT methylated and unmethylated tumors exhibited a distinct TME composition, with a significant higher number of perivascular CD8+ lymphocytes (p = 0.002), intratumoral CD8+ lymphocytes (p = 0.0024) and perivascular CD4+ lymphocytes (p = 0.014) in MGMT unmethylated tumors. PD-L1 expression in tumor cell surface was observed in four tumors (13.3%), and PD1 expression in infiltrating T lymphocytes was observed in nine (30%) tumors, with predominantly perivascular distribution. Conclusions: MGMT methylated and unmethylated tumors exhibit different immune profiles, likely reflecting the different biology of these tumors. The expression of PD-L1 in GBM IDH-wt patients is confined to a small subpopulation. While we found a significant association between low CD4+ lymphocyte density (≤10%) and survival, given the small numbers of our cohort, the prognostic value of CD4+ lymphocyte density will need to be validated in large-scale studies.
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Fenoglio, Daniela, Liliana Belgioia, Alessia Parodi, Francesco Missale, Almalina Bacigalupo, Alison Tarke, Fabiola Incandela, et al. "Development of Exhaustion and Acquisition of Regulatory Function by Infiltrating CD8+CD28− T Lymphocytes Dictate Clinical Outcome in Head and Neck Cancer." Cancers 13, no. 9 (May 6, 2021): 2234. http://dx.doi.org/10.3390/cancers13092234.

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Head and neck squamous cell carcinoma (HNSCC) has a poor clinical outcome despite the presence of a rich CD8+ T cell tumor infiltrate in the majority of patients. This may be due to alterations of tumor infiltrating CD8+ T cells. Here, we performed a characterization of HNSCC infiltrating CD8+ T cells in a cohort of 30 patients. The results showed that differential intratumoral frequency of CD8+CD28+ T cells, CD8+CD28− T cells, and CD8+CD28−CD127−CD39+ Treg distinguished between HNSCC patients who did or did not respond to treatment. Moreover, high PD1 expression identified a CD8+CD28− T cell subpopulation, phenotypically/functionally corresponding to CD8+CD28−CD127−CD39+ Treg, which showed a high expression of markers of exhaustion. This observation suggests that development of exhaustion and acquisition of regulatory properties may configure the late differentiation stage for intratumoral effector T cells, a phenomenon we define as effector-to-regulatory T cell transition.
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Wessel, Remziye E., Nardin Ageeb, Joseph M. Obeid, Ileana S. Mauldin, Kate A. Goundry, Gabriel F. Hanson, Mahdin Hossain, et al. "Spatial colocalization and combined survival benefit of natural killer and CD8 T cells despite profound MHC class I loss in non-small cell lung cancer." Journal for ImmunoTherapy of Cancer 12, no. 9 (September 2024): e009126. http://dx.doi.org/10.1136/jitc-2024-009126.

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BackgroundMajor histocompatibility complex class I (MHC-I) loss is frequent in non-small cell lung cancer (NSCLC) rendering tumor cells resistant to T cell lysis. NK cells kill MHC-I-deficient tumor cells, and although previous work indicated their presence at NSCLC margins, they were functionally impaired. Within, we evaluated whether NK cell and CD8 T cell infiltration and activation vary with MHC-I expression.MethodsWe used single-stain immunohistochemistry (IHC) and Kaplan-Meier analysis to test the effect of NK cell and CD8 T cell infiltration on overall and disease-free survival. To delineate immune covariates of MHC-I-disparate lung cancers, we used multiplexed immunofluorescence (mIF) imaging followed by multivariate statistical modeling. To identify differences in infiltration and intercellular communication between IFNγ-activated and non-activated lymphocytes, we developed a computational pipeline to enumerate single-cell neighborhoods from mIF images followed by multivariate discriminant analysis.ResultsSpatial quantitation of tumor cell MHC-I expression revealed intratumoral and intertumoral heterogeneity, which was associated with the local lymphocyte landscape. IHC analysis revealed that high CD56+cell numbers in patient tumors were positively associated with disease-free survival (HR=0.58, p=0.064) and overall survival (OS) (HR=0.496, p=0.041). The OS association strengthened with high counts of both CD56+and CD8+cells (HR=0.199, p<1×10−3). mIF imaging and multivariate discriminant analysis revealed enrichment of both CD3+CD8+T cells and CD3–CD56+NK cells in MHC-I-bearing tumors (p<0.05). To infer associations of functional cell states and local cell–cell communication, we analyzed spatial single-cell neighborhood profiles to delineate the cellular environments of IFNγ+/–NK cells and T cells. We discovered that both IFNγ+NK and CD8 T cells were more frequently associated with other IFNγ+lymphocytes in comparison to IFNγ–NK cells and CD8 T cells (p<1×10–30). Moreover, IFNγ+lymphocytes were most often found clustered near MHC-I+tumor cells.ConclusionsTumor-infiltrating NK cells and CD8 T cells jointly affected control of NSCLC tumor progression. Coassociation of NK and CD8 T cells was most evident in MHC-I-bearing tumors, especially in the presence of IFNγ. Frequent colocalization of IFNγ+NK cells with other IFNγ+lymphocytes in near-neighbor analysis suggests NSCLC lymphocyte activation is coordinately regulated.
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Xu, Yangmei, Suzhen Lan, and Qiuhong Zheng. "Prognostic significance of infiltrating immune cell subtypes in invasive ductal carcinoma of the breast." Tumori Journal 104, no. 3 (May 8, 2018): 196–201. http://dx.doi.org/10.5301/tj.5000624.

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Purpose: To explore the correlation between tumor-infiltrating immune cell subsets and breast cancer prognosis. Materials and methods: Specimens of 102 patients with invasive ductal carcinoma of the breast were analyzed for immune-related markers (CD8, CD20, FOXP3 and CD68). The number of positive cells in the 3 most highly stained intratumoral stroma areas of the primary tumor was counted. The mean number was calculated and used to divide patients into 2 groups for each marker (CD8-high/CD8-low, CD20-high/CD20-low, FOXP3-high/FOXP3-low, and CD68-high/CD68-low). Results: Kaplan-Meier survival analysis showed (a) for all patients that high tumor-infiltrating CD8+ and CD20+ B lymphocytes, low tumor-infiltrating FOXP3+ regulatory T cells (Tregs), and CD68+ macrophages all increased OS and DFS (p<0.05); (b) for both the 35 ER-negative and 45 lymph–node-negative patients, high CD8+ cytotoxic T lymphocytes (CTLs) increased OS and DFS (p<0.05). Multivariate analysis of OS and DFS showed that for all patients high CD8+ CTLs and low FOXP3+ Tregs were related to good OS and DFS (p<0.05). Conclusion: High numbers of tumor-infiltrating CD8+ and low numbers of FOXP3+ T lymphocytes both could function as potential independent prognostic markers for invasive ductal breast carcinoma.
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De Logu, Francesco, Francesca Galli, Romina Nassini, Filippo Ugolini, Sara Simi, Mara Cossa, Clelia Miracco, et al. "Digital Immunophenotyping Predicts Disease Free and Overall Survival in Early Stage Melanoma Patients." Cells 10, no. 2 (February 17, 2021): 422. http://dx.doi.org/10.3390/cells10020422.

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Background: the prognostic significance of tumor infiltrating lymphocytes (TILs) in intermediate/thick primary cutaneous melanoma (PCM) remains controversial, partially because conventional evaluation is not reliable, due to inter-observer variability and diverse scoring methods. We aimed to assess the prognostic impact of the density and spatial distribution of immune cells in early stage intermediate/thick PCM. Materials and Methods: digital image acquisition and quantitative analysis of tissue immune biomarkers (CD3, CD4, CD8, CD68, PD-L1, CD163, FOX-P3, and PD-1) was carried out in a training cohort, which included patients with primary PCM ≥ 2 mm diagnosed, treated, and followed-up prospectively in three Italian centers. Results were validated in an independent Italian cohort. Results: in the training cohort, 100 Stage II–III melanoma patients were valuable. At multivariable analysis, a longer disease free survival (DFS) was statistically associated with higher levels of CD4+ intratumoral T-cells (aHR [100 cell/mm2 increase] 0.98, 95%CI 0.95–1.00, p = 0.041) and CD163+ inner peritumoral (aHR [high vs. low] 0.56, 95%CI 0.32–0.99, p = 0.047). A statistically significant longer DFS (aHR [high-high vs. low-low] 0.52, 95%CI 0.28–0.99, p = 0.047) and overall survival (OS) (aHR [high-high vs. low-low] 0.39, 95%CI 0.18–0.85, p = 0.018) was found in patients with a high density of both intratumoral CD8+ T-cells and CD68+ macrophages as compared to those with low density of both intratumoral CD8+ T-cells and CD68+ macrophages. Consistently, in the validation cohort, patients with high density of both intratumoral CD8+ and CD3+ T-cells were associated to a statistically better DFS (aHR[high-high vs. low-low] 0.24, 95%CI 0.10–0.56, p < 0.001) and those with high density of both intratumoral CD8+ and CD68+ were associated to a statistically longer OS (aHR[high-high vs. low-low] 0.28, 95%CI 0.09–0.86, p = 0.025). Conclusion: our findings suggest that a specific preexisting profile of T cells and macrophages distribution in melanomas may predict the risk of recurrence and death with potential implications for the stratification of stage II–III melanoma patients.
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Wang, Li-Xin, Suyu Shu, Mary L. Disis, and Gregory E. Plautz. "Adoptive transfer of tumor-primed, in vitro–activated, CD4+ T effector cells (TEs) combined with CD8+ TEs provides intratumoral TE proliferation and synergistic antitumor response." Blood 109, no. 11 (June 1, 2007): 4865–76. http://dx.doi.org/10.1182/blood-2006-09-045245.

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Abstract The importance of CD4+ Th1 cells during the effector phase of the antitumor response has been overshadowed by emphasis on CD8+ cytotoxic T lymphocytes (CTLs). To determine their respective functions, we purified antigen-primed T cells from tumor-draining lymph nodes and separately activated CD4+ and CD8+ subsets in vitro. Adoptive transfer of CD4+ T effector cells (TEs) combined with CD8+ TEs provided synergistic therapy for mice bearing subcutaneous, intracranial, or advanced pulmonary metastases. CD4+ TEs augmented IFN-γ production by CD8+ TEs when cells were stimulated by tumor digest–containing antigen-presenting cells (APCs). CD4+ TEs infiltrated and proliferated extensively in pulmonary tumors, while also stimulating tumor antigen–specific CD8+ T cells. By contrast, CD8+ TEs showed minimal intratumoral proliferation in the absence of CD4+ cells or when systemically transferred CD4+ cells were prevented from infiltrating pulmonary tumors by pretreatment with pertussis toxin. Irradiation of CD4+ T cells immediately prior to adoptive transfer abrogated their intratumoral proliferation and direct antitumor efficacy but did not block their capacity to stimulate intratumoral CD8+ TE proliferation or tumor regression. These results highlight the importance of cross-presentation of tumor antigens during the effector phase of immunotherapy and suggest that approaches to stimulate CD4+ TE function and boost APC cross-presentation within tumors will augment cancer immunotherapy.
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Dissertations / Theses on the topic "Lymphocytes T CD8 intratumoraux"

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Cinier, Justine. "Importance et potentiel thérapeutique d'un nouveau couple récepteur-ligand dans l'inhibition des lymphocytes T CD8 par les lymphocytes T régulateurs dans les tumeurs." Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10336.

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La présence de lymphocytes T (LT) CD8 dans le microenvironnement tumoral (TME) corrèle avec un bon pronostic dans de nombreux types de cancers solides. En périphérie, les LT régulateurs (Treg) jouent un rôle majeur dans le maintien d’une homéostasie immunitaire et empêchent le développement de pathologies auto-immunes. Néanmoins, dans le TME, les Treg (TA-Treg) ont un impact pronostic défavorable en inhibant la réponse immunitaire antitumorale. Sur le plan thérapeutique, il est indispensable d’éliminer ces TA-Treg ou leur fonction pour restaurer une réponse immunitaire antitumorale efficace. Pour cela, il reste important d’identifier des molécules membranaires permettant le ciblage sélectif de ces TA-Treg sans affecter les Treg périphériques pour éviter toute réaction auto-immune. L’analyse de données publiques de scRNA-seq comparant les LT (Treg, CD8, CD4) de tumeur, tissu sain et sang, a permis d’identifier l’expression sélective de CD177 par une population de TA-Treg dans plusieurs tumeurs solides. Si cette glycoprotéine est impliquée dans l’extravasation et la survie des neutrophiles, son rôle sur les Treg n’a été que peu décrit hormis dans quelques études confirmant l’expression de CD177 sur les TA-Treg dans plusieurs types tumoraux et montrant un effet suppresseur de ces TA-Treg CD177+ dans des cocultures avec des LT CD4 naïfs. Néanmoins, la caractérisation phénotypique et fonctionnelle de ces Treg reste peu explorée. CD177 interagit avec PECAM-1 qui est impliqué dans la transmigration des LT par interaction homophilique des domaines extracellulaires distaux immunoglobuline-like (IgD1/D2) avec les cellules endothéliales. De plus, il a été décrit que l’interaction avec le IgD6 extracellulaire de PECAM-1, zone de liaison de CD177, transmet un signal négatif via les motifs intracellulaires inhibiteurs (ITIM) et le recrutement de SHP2 qui bloque la signalisation TCR et la prolifération des LT. La réanalyse de données publiques de scRNA-seq de LT intra-tumoraux montre la restriction de l’expression de PECAM1 à des clusters de LT CD8 effecteurs mémoires suggérant qu’ils pourraient être la cible de la fonction immunosuppressive des Treg CD177+ dans le TME. Ainsi, dans l’objectif d’identifier un mécanisme de suppression des Treg spécifique des LT CD8 effecteurs dans l’environnement tumoral il est important de caractériser de manière approfondie ces TA-Treg CD177+ et d’identifier leurs interactions avec les LT CD8 PECAM-1+ dans le TME et leur impact sur la fonction de ces LT CD8. Ce travail de thèse a permis de démontrer, dans plusieurs types tumoraux, que CD177 identifie une population de Treg spécifiques de la tumeur, avec un phénotype activé. PECAM-1, la cible de CD177, est exprimé dans le TME par des LT CD8 effecteurs polyfonctionnels (GzmK, IFNү, TNFα), à forte capacité de prolifération. In situ sur coupe de tumeurs, des analyses de multi-immunofluorescence ont montré la colocalisation des Treg CD177+ et des LT CD8 PECAM-1+ au niveau du stroma tumoral, suggérant un lien entre ces deux populations. Par ailleurs, l’engagement de PECAM-1 IgD6, domaine de liaison de CD177, réduit l’activation et les fonctions des LT CD8 PECAM-1+ induites par le signal TCR en diminuant pZAP-70 et la sécrétion d’IFNү. Enfin, des premiers résultats sur tumeur ont montré que la culture de LT CD8 avec des TA-Treg CD177+ diminue la prolifération et la sécrétion d’IFNγ par les LT CD8 PECAM-1+ et l’ajout d’un anti-CD177 permet de lever en partie cette inhibition, suggérant le rôle de l’axe [CD177/PECAM-1] dans l’inhibition des LT CD8 PECAM-1+ par les TA-Treg CD177+. L’interaction [CD177/PECAM-1] représente la première mise en évidence d’un couple récepteur/ligand membranaire impliqué dans l’inhibition sélective des LT CD8 effecteurs par les TA-Treg dans le TME et CD177 apparait comme une cible prometteuse pour lever spécifiquement la suppression médiée par les Treg dans le TME sans altérer ceux de la périphérie
The presence of CD8 T cells in the tumor microenvironment (TME) correlates with good prognosis in many types of solid cancers. In the periphery, regulatory T cells (Treg) play a major role in maintaining immune homeostasis and preventing the development of autoimmune pathologies. However, in the TME, Treg (TA-Treg) have an unfavorable prognostic impact by inhibiting the anti-tumor immune response. Therapeutically, it is essential to eliminate these TA-Treg or their function to restore an effective anti-tumor immune response. For this, it remains important to identify membrane molecules allowing the selective targeting of these TA-Treg without affecting the Treg present in the periphery to avoid any autoimmune reaction. The analysis of public scRNA-seq data comparing T cells (Treg, CD8, CD4) from tumor, healthy tissue and blood, made it possible to identify the selective expression of CD177 by a subpopulation of TA-Treg in different solid tumors. If this glycoprotein is known for its involvement in the extravasation and survival of neutrophils, its role on Treg has been little described except in a few studies confirming the expression of CD177 on TA-Treg of several types of tumors and showing a suppressive impact of CD177+ TA-Treg in cocultures with naïve CD4 T cells. However, the phenotypic and functional characterization of these Treg remains little explored. CD177 interacts with PECAM-1 which is involved in T cells transmigration through homophilic interaction of distal extracellular immunoglobulin-like domains (IgD1/D2) with endothelial cells. Furthermore, it has been described that interaction with extracellular PECAM-1 IgD6, CD177 binding site, transmits a negative signal via inhibitory intracellular motifs (ITIM) and recruitment of SHP2 which blocks TCR signaling and the proliferation of T cells. Reanalysis of public scRNA-seq data from intra-tumoral T cells shows the restriction of PECAM1 expression to clusters of memory effector CD8 T cells suggesting that they could be the target of the immunosuppressive function of CD177+ Treg in the TME. Thus, with the aim of identifying a Treg suppression mechanism specific to effector CD8 T cells in the TME, it is important to characterize in depth these CD177+ TA-Treg and to identify their interactions with PECAM-1+ CD8 T cells in the TME and their impact on the function of these CD8 T cells. This thesis work demonstrated, in several tumor types, that CD177 identifies a population of TA- Treg, with an activated phenotype. PECAM-1, the target of CD177, is expressed in the TME by polyfunctional effector CD8 T cells (GzmK, IFNγ, TNFα) with a high proliferation capacity. In situ on tumor sections, multi-immunofluorescence analyses showed the colocalization of CD177+ Treg and PECAM-1+ CD8 T cells in the tumor stroma, suggesting a link between these two populations. Furthermore, engagement of PECAM-1 IgD6, CD177 binding domain, reduces the activation and functions of PECAM-1+ CD8 T cells induced by the TCR signal by decreasing pZAP-70 and IFNү secretion. Finally, initial results on tumors have shown that the culture of CD8 T cells with CD177+ TA-Treg reduces the proliferation and secretion of IFNγ by PECAM-1+ CD8 T cells and the addition of an anti-CD177 makes it possible to partly rescue this inhibition, suggesting the role of the [CD177/PECAM-1] axis in the inhibition of PECAM-1+ CD8 T cells by CD177+ TA-Treg. The [CD177/PECAM-1] interaction represents the first demonstration of a membrane receptor/ligand pair involved in the selective inhibition of CD8 T cells effectors by TA-Treg in the TME and CD177 appears as a promising target to specifically raise suppression mediated by TA-Treg in the TME without altering those in the periphery
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Mokrani, M'barka. "CD103 : du gène à la protéine : Etude de la régulation et de la signalisation de l’intégrine αE(CD103)β7 exprimée par les lymphocytes T CD8+ intratumoraux." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T071.

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L’élucidation des mécanismes permettant l’optimisation de la réponse immunitaire antitumorale correspond à un enjeu majeur pour le développement de stratégies d’immunothérapie efficace. En effet, les réponses immunitaires antitumorales se traduisent rarement par l’éradication de la tumeur. Dans ce contexte, les travaux antérieurs de mon équipe ont démontré que l’interaction de l’intégrine αE(CD103)β7, souvent exprimée par les lymphocytes infiltrant la tumeur (TIL), avec son ligand E-cadhérine, à la surface des cellules tumorales épithéliales, joue un rôle majeur dans la potentialisation de l’activité lytique des cellules T en induisant la polarisation et l’exocytose des granules cytotoxiques. Nos résultats ont indiqué aussi que le TGF-β1, souvent abondant dans les tumeurs, joue un rôle déterminant dans cette induction suite à l’engagement du récepteur des cellules T. Dans ce contexte, nous avons cherché à comprendre les mécanismes de régulation du gène ITGAE qui codent la sous-unité alphaE de l’intégrine CD103. Nos résultats ont montré que les facteurs transcriptionnels Smad2, Smad3 et NFAT-1 sont impliqués dans la régulation de l’expression de la sous-unité αE(CD103). En effet, une costimulation avec du TGF-β1 recombinant et un anticorps anti-CD3 d’un clone T CD103- induit l’expression de cette intégrine qui est accompagnée d’une translocation dans le noyau de Smad2, Smad3 et NFAT-1 qui sont cytoplasmiques à l’état basal. L’inhibition spécifique de ces facteurs transcriptionnels inhibe l’expression de CD103 et abroge le potentiel lytique du clone T vis à vis de sa cible tumorale autologue. De plus, nous avons identifié deux séquences régulatrices du gène ITGAE humain, un promoteur proximal et un enhancer. Par ailleurs, mon équipe a récemment montré que l’interaction de CD103 à la surface des TIL avec une molécule E-cadhérine recombinante est suffisante pour induire la polarisation des granules cytolytiques par un mécanisme dépendant de la PLC-g1 et ERK et que cette intégrine possède non seulement une fonction d’adhérence, mais aussi une fonction de costimulation du signal TCR des TIL antitumoraux. Nous avons cherché à mieux comprendre la signalisation de l’intégrine CD103, en identifiant les domaines intracytoplasmiques de la sous-unité αE impliqués dans son activation. Nous avons ainsi construit une protéine de fusion CD103-GFP et plusieurs mutants du domaine intracytoplasmique de la sous-unité αE qui ont été ensuite transfectés dans la lignée Jurkat Tag CD103-/beta7+. Nos résultats ont montré que le domaine intracytoplasmique de la chaîne alphaE n’est pas nécessaire à la reconnaissance du ligand, la E-cadhérine. Par contre, nous avons montré que ce domaine est impliqué dans le phénomène de clustering de l’intégrine et dans sa polarisation à la zone de contact avec des billes couvertes avec la E-cadhérine-Fc. Nous avons identifié un domaine de 8 acides aminés (ESIRKAQL), contenant une sérine en position 1163 potentiellement phosphorylable, et qui est indispensable pour la signalisation de l’intégrine. De plus, nos travaux ont montré que ce domaine ESIRKAQL, est nécessaire pour la phosphorylation de la ERK1/2 et PLC-g1. Ainsi, une meilleure compréhension des mécanismes moléculaires régulant les fonctions de CD103 pourrait contribuer au développement et à l’amélioration de la réponse antitumorale exercée par les CTL
The elucidation of mechanisms for optimizing the antitumor immune response is a major challenge for the development of strategies for effective immunotherapy. Indeed, the anti-tumor immune responses rarely result in the eradication of the tumor. In this context, the previous work of my team have shown that the interaction of integrin αE(CD103)β7, often expressed by tumor infiltrating lymphocytes (TIL) with its ligand E-cadherin at the cell surface tumor epithelial cells, plays a major role in the potentiation of the lytic activity of T cells by inducing polarization and exocytosis of cytotoxic granules. Our results also indicated that TGF-β1, often abundant in tumors, plays a key role in the induction due to the commitment of the T cell receptor. In this context, we sought to understand the mechanisms regulating ITGAE gene encoding the subunit αE of integrin. Our results showed that the transcription factors Smad2, Smad3 and NFAT-1 are involved in regulating the expression of subunit αE(CD103)β7. Indeed, costimulation with recombinant TGF-β1 and anti-CD3 antibody induces on T cell clone CD103- the expression of this integrin ant the translocation into the nucleus of Smad2, Smad3 and NFAT-1 that are cytoplasmic at baseline. Specific inhibition of these transcription factors inhibits the expression of CD103 and repeals the lytic potential of cloned T with respect to the autologous tumor target. In addition, we identified two regulatory sequences of human ITGAE gene, proximal promoter and enhancer. In addition, my team has recently shown that the interaction of CD103 on the surface of TIL with a recombinant molecule E-cadherin is sufficient to induce the polarization of cytolytic granules by ERK and PLC-γ1 pathway thus this integrin has not only a function of adherence, but also a function of costimulatory signal TCR of TIL. We sought to better understand the signaling of integrin CD103, by identifying the cytoplasmic domains of the subunit αE involved in its activation. We have constructed a fusion protein CD103-GFP and several mutants of intracytoplasmic domain of the subunit αE which were then transfected into the Jurkat Tag cell line CD103-/ β7+. Our results showed that the intracytoplasmic domain of CD103 is not necessary for ligand recognition, E-cadherin. By cons, we have shown that this area is involved in the phenomenon of clustering of integrin and its polarization to the contact area with balls covered with E-cadherin-Fc. We have identified a range of 8 amino acids (ESIRKAQL) containing a potentially phosphorylatable serine in position 1163, which is essential for integrin signaling. In addition, our work has shown that this area ESIRKAQL is necessary for the phosphorylation of ERK1/2 and PLC-g1. Thus, a better understanding of the molecular mechanisms that regulate the functions of CD103 may contribute to the development and improvement of the antitumor response exerted by CTL
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Badoual, Cécile. "Rôle pronostique des lymphocytes T CD4+CD25+ intratumoraux et analyse des mécanismes de production du CD25 soluble dans les tumeurs des voies aéro-digestives supérieures." Paris 6, 2005. http://www.theses.fr/2005PA066467.

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Granier, Clémence. "Expression de récepteurs inhibiteurs sur les lymphocytes T infiltrant les tumeurs du rein : signification biologique et clinique Multiplexed immunofluorescence analysis and quantification of intratumoral PD-1+ Tim-3+ CD8+ T cells Tim-3 expression on tumor-infiltrating PD-1+CD8+ T cells correlates with poor clinical outcome in renal cell carcinoma." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB183.

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L'expression de récepteurs inhibiteurs tels PD-1, TIM-3, LAG-3, TIGIT sur les lymphocytes T participe à l'immunosuppression dans l'environnement tumoral. Le ciblage de PD-1 par les immunothérapies anti-PD-1/PD-L1 notamment révolutionne depuis peu la prise en charge de nombreux types de cancers en particulier dans le mélanome, cancer du poumon et aussi du rein. Dans la plupart des cancers comme dans celui du poumon et le mélanome, l'infiltrat CD8 et la réponse Th-1/IFN-gamma sont associés à un meilleur pronostic, contrairement aux tumeurs du rein et aux hémopathies. Les travaux de ma thèse s'intéressent à la caractérisation de l'expression des récepteurs inhibiteurs des lymphocytes, notamment PD-1 et TIM-3 dans le carcinome rénal et dans le lymphome. Mes travaux de thèse ont été réalisés avec des outils d'exploration du microenvironnement tumoral permettant une analyse multiplexe de nombreux paramètres in situ. En théorie jusqu'à 7 protéines peuvent être mises en évidence à la fois, j'ai pu mettre au point des comarquages de 4 protéines membranaires et/ ou nucléaires + Dapi ainsi que la détection d'ARN in situ dans les tumeurs. L'utilisation d'un outil technologique de microscopie à fluorescence multispectrale a permis une étude fine de la coexpression de PD-1 et Tim-3 sur les lymphocytes T CD8 (LT-CD8) grâce à la visualisation aisée de la colocalisation de ces 3 marqueurs. De la même façon, j'ai mis en évidence de l'expression de leurs ligands PD-L1 et Galectin-9 (Gal-9) dans l'environnement des tumeurs du rein. J'ai démontré que la co-expression de Tim-3 et PD-1 sur les CD8 dans le carcinome rénal avait un rôle délétère aussi bien sur le plan (i) fonctionnel puisque les LT-CD8 sécrétaient moins d'IFN-gamma, (ii) et clinique puisque les patients présentant un infiltrat de LT-CD8 double positifs pour PD-1 et TIM-3 récidivaient plus fréquemment. La présence des ligands PD-L1 et Gal-9 a été mise en évidence dans l'environnement tumoral laissant suggérer des interactions possibles avec les récepteurs inhibiteurs exprimés par les LT. J'ai également caractérisé les LT-CD8 PD-1+ TIM-3+ dans les lymphomes en combinant un marquage CD20 (quadruple + Dapi). Selon le type de lymphome, TIM-3 était coexprimé avec PD-1 à la surface des CD8 et plus ou moins au contact avec les cellules lymphomateuses CD20+. D'autre part, lorsque TIM-3 était coexprimé, les LT-CD8 étaient plus volontiers proliférant (comarquage Ki-67) en comparaison aux PD-1+ TIM-3-. Afin de poursuivre dans la caractérisation Th-1/IFN-gamma, j'ai élaboré la mise au point de la détection d'ARN dans les lymphocytes T in situ dans la tumeur, permettant de faire des liens avec leur fonctionnalité. Au total mes travaux de thèse ont permis de mettre en évidence des biomarqueurs immunologiques composites en lien avec l'expression des récepteurs inhibiteurs PD-1 et/ou TIM-3 et la perte de fonctionnalité (IFN-gamma) des lymphocytes T intratumoraux
It has been mainly described that the inhibitory receptors coexpression (PD-1, TIM-3, LAG-3, TIGIT) by lymphocytes in the tumor microenvironment (TME) induces a local immunosuppression. Targeting these receptors particularly PD-1 and its ligand PD-L1 is of great clinical benefit in cancer many types treatment (melanoma, renal and lung cancer in particular). In the most cases of cancer, like melanoma and lung cancer, a CD8-T cell and Th-1/IFN-gamma response is of good prognosis. But this is not the case in renal cancer and in hemopathies. My PhD work attempts to characterize clinical and biological implication of PD-1 and TIM-3 expression by intra-tumor lymphocytes in the setting of renal cancer and lymphoma. My PhD work has been conducted thanks to new methods of multiplexed characterization of the TME. Multispectral immunofluorescence lead to identify 7 parameters at the same time, and in this study I elaborated the identifications of lymphocytes markers in situ within the tumor: 4 membrane and/or nuclear proteins + nuclei (Dapi counterstain) and also coupled with the RNA detection. This tool allows me to accurately study the coexpression of PD-1 and TIM-3 at the CD8-T cell surface thanks to colocalisation identification and counting of these 3 markers. With the same method, I found that PD-L1 and Gal-9, which are PD-1 and TIM-3 ligands, were also expressed in the TME of renal carcinoma. I found that the coexpression of TIM-3 together with PD-1 in the CD8-T cells had a double relevance (i) at functional level, CD8-T cells were less able to secrete gamma-IFN (ii) at clinical level, patients harboring a higher infiltrate were more likely to relapse. The presence of PD-L1 and Gal-9 suggested interactions with inhibitory receptors of T cells. I also characterized CD8-T cells expressing PD-1 and TIM-3 in lymphomas, combining a CD20 staining (quadruple staining + Dapi). TIM-3 was more or less expressed depending of the lymphoma type near to CD20+ cells. TIM-3 PD-1 CD8-T cells were more likely Ki-67+ compared to TIM-3- cells, suggesting a more proliferative capacity. In order to continue the characterization of the Th-1/gamma-IFN-gamma immune response, I elaborate a technic to detect the gamma-IFN RNA in situ, together with lymphocytes staining, allowing the exploration of functionality within the tumor. To summarize, during my PhD work I could characterize composite immune biomarkers linked to the functionality of CD8-T cell and gamma-IFN Th-1 response
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Jacquet, Alexandra. "Etude de la réponse T CD4+ antitumorale : régulation de l'expansion et de l'accumulation intratumorale et établissement de nouveaux modèles de tumeurs transplantées et spontanées." Paris 5, 2009. http://www.theses.fr/2009PA05T010.

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La destruction de tumeurs par le système immunitaire est très rare chez l'Homme. Afin de mieux comprendre cette absence de rejet de nombreuses études ont été/sont menées chez la souris grâce à des modèles de tumeurs transplantées. Ces modèles présentent de nombreux inconvénients pour l'étude des réponses immunes anti-tumorales dus, en particulier, à la libération d'une grande quantité d'antigène par les cellules tumorales mourantes ou mortes dans un contexte traumatique lors de l'implantation des tumeurs. Nous avons établi un modèle de tumeur spontanée dans lequel il est possible de faire exprimer un antigène nominal uniquement par les cellules tumorales ainsi que des modèles de tumeurs transplantées dans lesquels l'expression de l'antigène peut être induite à distance de l'implantation évitant ainsi/les sources d'artefacts. Nous pouvons désormais étudier dans de meilleures conditions les relations entre tumeur et système immunitaire.
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Zaragoza, Bruno. "Rôle des lymphocytes T CD4+ dans l'homéostasie des lymphocytes T CD8+." Paris 6, 2009. http://www.theses.fr/2009PA066313.

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Dans une première partie, nous nous sommes concentrés sur l’homéostasie des lymphocytes T CD4+. Nous montrons que le pourcentage de cellules T CD4+CD25+ parmi les cellules T CD4+ est indexé au nombre de cellules IL-2+. Nous avons découvert que la conversion des cellules T CD4+CD25- en cellules T CD4+CD25+ était possible mais inhibé par la présence de cellules T CD4+CD25+. Enfin, dans deuxième partie, nous avons étudié le rôle des lmphocytes T CD4+ dans l’homéostasie des lymphocytes T CD8+. Le co-transfert de cellules T CD4+ naïves accroît la prolifération dûe à la lymphopénie des cellules T CD8+ augmentant de 10 à 20 fois le nombre de cellules T CD8+CD44+CD62Llow récupérées en périphérie sans modifier le nombre de cellules T CD8+CD44+CD62Lhigh. Nous montrons que l’effet auxiliaire est dépendant de l'expression de la molécule CD40 par les cellules non-B de l'hôte et de l’expression de l’IL-2 par les cellules T CD4+ naïves.
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Tyznik, Aaron Jacob. "CD4+ T cell help for CD8+ T cell responses /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8314.

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Veiga, Fernandez Henrique. "Caractérisation des propriétés des cellules T CD8 mémoires." Paris 5, 2002. http://www.theses.fr/2002PA05N127.

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Nous avons démontré que les cellulles T CD8 mémoires sont plus efficaces que les cellules nai͏̈ves après stimulation antigénique in vivo. Cette caractéristique unique des cellules mémoires est due à leurs propriétés de division et de différenciation en fonctions effectrices. Après stimulation antigénique, les cellules mémoires, comparées aux cellules naives se divisent plus tôt, ont un taux de division supérieur et un taux de perte réduit. Ces propriétés expliquent l'expansion trés importante des cellules mémoires après stimulation antigénique in vivo. Pour déterminer les mécanismes responsables de ces capacités uniques nous avons étudié l'arrêt et la progression dans le cycle cellulaire des cellules nai͏̈ves. .
We showed that on a per cell basis memory T cells are more efficient in dealing with the antigenin vivo than their counter partners, the naive T cells. This different capacity is due to qualitative differences of memory T cells related to division and differentiation into effector functions. Compared to na^ive T cells, memory cells divide after a shorter lag time, have an increased division rate and a lower loss rate. Altogether, these parameters justify the efficient expansion of memory T cells upon in vivo stimulation. To assess the mechanisms underlying these unusual proliferative capacities, we studied the cell cycle arrest and progression of nai͏̈ve and memory T cells ex vivo. Despite the high levels of D cyclins and CDKs, memory T cells
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Mashishi, Tumelo Nkoenyana. "Functional characterisation of HIV-1 specific CD8+ T lymphocytes." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445783.

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Fornairon, Sophie. "Expression des cytokines dans les lymphocytes T CD8+ / CD57+." Paris 7, 1994. http://www.theses.fr/1994PA072063.

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Books on the topic "Lymphocytes T CD8 intratumoraux"

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Barker, Brianne Raye. Critical role for Interleukin-21 in antiviral CD8-positive T Lymphocyte responses. 2009.

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Sen, Pritha. Clonal diversity of epitope-specific CD8+ T lymphocytes in rhesus monkeys following vaccination and simian-human immunodeficiency virus challenge. 2008.

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Veskler, Barbara A. New Research On Immunology. Nova Biomedical Books, 2005.

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Bauer, Jan, and Christian G. Bien. Rasmussen Encephalitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0096.

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Rasmussen encephalitis (RE) is a rare epileptic disorder that is characterized by the presence of unihemispheric seizures coinciding with inflammation. The disease mostly presents in children. Clinically, patients often reach a residual stage with drug resistant seizures and severe neurological deficits. Pathologically, at this stage, the brain shows variable neuronal loss. The etiology is unknown but the infiltration of large numbers of CD8 positive T lymphocytes suggests that this is an autoimmune disease. Treatment consists of anti-inflammatory therapy (IVIG or tacrolimus), which, however, does not reduce the drug-resistant seizures. Therefore, hemisperectomy is the most effective treatment of RE.
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Grom, Alexei A., and Athimalaipet V. Ramanan. Macrophage activation syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0168.

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Macrophage activation syndrome (MAS) is a life-threatening condition caused by excessive activation and proliferation of T lymphocytes and haemophagocytic macrophages. Although MAS has been reported in association with almost any rheumatic disease, it is by far most common in systemic juvenile idiopathic arthritis. Flares of the underlying disease or infection are most common triggers of MAS. The pathognomonic feature of MAS is typically found in bone marrow: numerous, well-differentiated macrophagic histiocytes phagocytosing normal haematopoietic elements. The expansion of these histiocytes leads to a massive systemic inflammatory reaction associated with three cardinal clinical features: severe cytopenias, liver dysfunction, and coagulopathy consistent with disseminated intravascular coagulation. Clinically, MAS is strikingly similar to the autosomal recessive disorders collectively known as familial haemophagocytic lymphohistiocytosis (FHLH). FHLH has been associated with various genetic defects affecting the cytolytic pathway. Cytolytic function is profoundly depressed in MAS patients as well, and this abnormality is caused by both genetic and acquired factors. Studies in animals suggest that uncontrolled expansion of activated CD8+ T lymphocytes secreting cytokines that activate macrophages is central to the pathophysiology of haemophagocytic syndromes. Consistent with this view, the combination of steroids and ciclosporin, an immunosuppressant that preferentially inhibits T lymphocytes, is an effective treatment for the majority of MAS patients. Patients in whom MAS remains active despite this treatment present a serious challenge and require more aggressive immunosuppression. However, in MAS triggered by infection, the optimal level of immunosuppression is difficult to determine. As a result, reported mortality rates reach 20%.
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Hasbun, Rodrigo, Richard Dunham, Joseph S. Kass, Rituparna Das, Karen Nunez-Wallace, Lydia J. Sharp, and Doris Kung. HIV-Associated Neurocognitive Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0038.

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HIV causes a chronic form of encephalitis (HIVE) that is clinically characterized by either dementia or mild neurocognitive impairment. Since the introduction of antiretroviral therapy in 1996, the incidence of HIV dementia has decreased by 50%, but the prevalence of mild neurocognitive disorder has increased up to 39%. HIVE is the result of direct microglial infection, interruption of trophic factors, or caused by inflammatory cytokines. HIV enters the brain primarily by the “Trojan horse mechanism”; it is carried by monocytes and lymphocytes that cross the blood–brain barrier. HIV has a predilection for the basal ganglia, deep white matter, and hippocampus, resulting in a subcortical dementia. HIV dementia is a diagnosis of exclusion and other co-infections, cerebrovascular disease, malnutrition, and drug abuse should be ruled out before making the diagnosis. In patients receiving antiretroviral therapy with immunological response, a novel condition termed CD8+ T cell encephalitis was recently described.
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Book chapters on the topic "Lymphocytes T CD8 intratumoraux"

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Tong, Joo Chuan. "CD8+ Cytotoxic T Lymphocytes (CTL)." In Encyclopedia of Systems Biology, 214. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_938.

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Lemonnier, François A. "Cloning CD8+ Cytolytic T Lymphocytes." In Antigen Processing, 279–96. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-218-6_21.

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Rich, Robert R., Edward J. Fox, and Medhat N. ElMasry. "Differentiation and Proliferation of CD8+ Suppressor T Lymphocytes." In Molecular Basis of Lymphokine Action, 59–71. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4598-8_6.

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Tanaka, Hirokazu, and Ichiro Taniuchi. "The CD4/CD8 Lineages: Central Decisions and Peripheral Modifications for T Lymphocytes." In Thymic Development and Selection of T Lymphocytes, 113–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/82_2013_323.

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Wagner, H., and K. Heeg. "Signal Requirements for the Primary Activation of Murine CD8 T Lymphocytes." In Progress in Immunology, 581–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_78.

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Mowat, A. Mcl, A. J. Edwards, and I. N. Crispe. "T cell receptor expression by CD8+ intraepithelial lymphocytes from mouse small intestine." In Advances in Mucosal Immunology, 83–85. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_21.

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Bhardwaj, Nina, Armin Bender, Noemi Gonzalez, Long Kim Bui, Maria C. Garrett, and Ralph M. Steinman. "Stimulation of Human Anti-Viral CD8+ Cytolytic T Lymphocytes by Dendritic Cells." In Advances in Experimental Medicine and Biology, 375–79. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1971-3_84.

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Shibata, Shinwa, Shigeru Kyuwa, Kosaku Fujiwara, Yutaka Toyoda, and Naoaki Goto. "Mouse Hepatitis Virus-Specific CD8+ Cytotoxic T Lymphocytes Induce Apoptosis in Their Target Cells." In Advances in Experimental Medicine and Biology, 109–11. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_17.

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Arbour, Nathalie, and Alexandre Prat. "Roles of CD4 and CD8 T Lymphocytes in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis." In Neuroinflammation, 39–52. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118732748.ch3.

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Fowlkes, B. J., D. Pardoll, T. Lantz, and F. Ramsdell. "Participation of CD4 and CD8 Accessory Molecules in the Development and Selection of T Lymphocytes." In Progress in Immunology, 282–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_38.

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Conference papers on the topic "Lymphocytes T CD8 intratumoraux"

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Ryan, RM, Q. Ahmed, CA D'Angelis, VH Kumar, S. Lakshminrusimha, LA Metlay, H. Wang, and GS Pryhuber. "CD8+ T-Lymphocytes in Infants with Bronchopulmonary Dysplasia (BPD)." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5976.

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Joseph, Robiya, Rama Soundararajan, Suhas Vasaikar, Fei Yang, Sevinj Isgandarova, Lin Tian, Monika Haemmerle, et al. "Abstract 3761: Regulation of metastasis by CD8 T lymphocytes." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3761.

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Joseph, Robiya, Rama Soundararajan, Suhas Vasaikar, Fei Yang, Sevinj Isgandarova, Lin Tian, Monika Haemmerle, et al. "Abstract 3761: Regulation of metastasis by CD8 T lymphocytes." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3761.

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Jiang, W., H. Hong, R. Juskevicius, D. A. Weidner, Y. Feng, L. V. Yang, J. Q. Lu, and X. H. Hu. "Study of 3D Structural Differences between CD4+ and CD8+ T lymphocytes." In Biomedical Optics. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/biomed.2014.bs3a.78.

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Hinks, Timothy, Bart Hilvering, Linda Stoger, Emanuele Marchi, Maryam Salimi, Rahul Shrimanker, Wie Lu, et al. "Type-2 CD8+ T lymphocytes responsive to PGD2/LTE4 in severe eosinophilic asthma." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa4927.

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Gohring, John T., and Xudong Fan. "Detection of CD4+ and CD8 + T-lymphocytes with the optofluidic ring resonator (OFRR) biosensor." In SPIE Defense, Security, and Sensing, edited by Hai Xiao, Xudong Fan, and Anbo Wang. SPIE, 2009. http://dx.doi.org/10.1117/12.818255.

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Wahlin, B., AE Fasth, K. Karp, K. Lejon, A. Södergren, and S. Wållberg-Jonsson. "THU0129 Cd8+cd28- t-lymphocytes are associated with subclinical atherosclerosis in patients with rheumatoid arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4364.

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Guo, Zhijun, David Owen, Pamela Rosato, David Masopust, Michael A. Farrar, and David A. Potter. "Abstract 3525: N1-hexyl-N5-benzyl-biguanide promotes proliferation of CD4+ and CD8+ T lymphocytes." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3525.

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Heeke, Christina, Anne-Mette Bjerregaard, Amalie Kai Bentzen, Marco Donia, Rikke Andersen, Marie Stentoft Svane, and Sine Reker Hadrup. "Abstract B015: T-cell recognition profiling of CD8+ T-cells in tumor-infiltrating lymphocytes expanded for adoptive cell transfer." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b015.

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Schirmer, M., C. Goldberger, C. Duftner, J. Clausen, and A. Falkenbach. "SAT0033 Enrichment of cd8+cd28- cytotoxic t cells in circulating lymphocytes of patients with ankylosing spondylitis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.385.

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Reports on the topic "Lymphocytes T CD8 intratumoraux"

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Banai, Menachem, and Gary Splitter. Molecular Characterization and Function of Brucella Immunodominant Proteins. United States Department of Agriculture, July 1993. http://dx.doi.org/10.32747/1993.7568100.bard.

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Abstract:
The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.
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