Relevant bibliographies by topics / Resident memory T lymphocytes

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Academic literature on the topic 'Resident memory T lymphocytes'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Resident memory T lymphocytes"

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Labuda, Jasmine C., Oanh H. Pham, Claire E. Depew, Kevin D. Fong, Bokyung Lee, Jordan A. Rixon, and Stephen J. McSorley. "Circulating immunity protects the female reproductive tract from Chlamydia infection." Proceedings of the National Academy of Sciences 118, no. 21 (May 17, 2021): e2104407118. http://dx.doi.org/10.1073/pnas.2104407118.

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Anatomical positioning of memory lymphocytes within barrier tissues accelerates secondary immune responses and is thought to be essential for protection at mucosal surfaces. However, it remains unclear whether resident memory in the female reproductive tract (FRT) is required for Chlamydial immunity. Here, we describe efficient generation of tissue-resident memory CD4 T cells and memory lymphocyte clusters within the FRT after vaginal infection with Chlamydia. Despite robust establishment of localized memory lymphocytes within the FRT, naïve mice surgically joined to immune mice, or mice with only circulating immunity following intranasal immunization, were fully capable of resisting Chlamydia infection via the vaginal route. Blocking the rapid mobilization of circulating memory CD4 T cells to the FRT inhibited this protective response. These data demonstrate that secondary protection in the FRT can occur in the complete absence of tissue-resident immune cells. The ability to confer robust protection to barrier tissues via circulating immune memory provides an unexpected opportunity for vaccine development against infections of the FRT.
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Han, Ji Won, and Seung Kew Yoon. "Tissue-Resident Lymphocytes: Implications in Immunotherapy for Hepatocellular Carcinoma." International Journal of Molecular Sciences 22, no. 1 (December 28, 2020): 232. http://dx.doi.org/10.3390/ijms22010232.

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Hepatocellular carcinoma (HCC) is a hard-to-treat cancer. The recent introduction of immune checkpoint inhibitors (ICIs) provided viable options to treat HCC, but the response rate is currently not sufficient. Thus, a better understanding of ICI-responding cells within tumors is needed to improve outcomes of ICI treatment in HCC. Recently, tissue-resident memory T (TRM) cells were defined as a subset of the memory T cell population; this cell population is actively under investigation to elucidate its role in anti-tumor immunity. In addition, the role of other tissue-resident populations such as tissue resident regulatory T (Treg) cells, mucosal associated invariant T (MAIT) cells, γδ T cells, and invariant natural killer T (iNKT) cells in anti-tumor immunity is also actively being investigated. However, there is no study that summarizes recent studies and discusses future perspectives in terms of tissue resident lymphocytes in HCC. In this review, we summarize key features of tissue-resident lymphocytes and their role in the anti-tumor immunity. Additionally, we review recent studies regarding the characteristics of tissue-resident lymphocytes in HCC and their role in ICI treatment and other immunotherapeutic strategies.
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Wu, Kang, Fei Wang, Guangwu Guo, Yuqing Li, Li-Jun Qiu, and Xuefeng Li. "CD4+ TSCMs in the Bone Marrow Assist in Maturation of Antibodies against Influenza in Mice." Mediators of Inflammation 2019 (January 10, 2019): 1–10. http://dx.doi.org/10.1155/2019/3231696.

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The bone marrow (BM) is not only a reservoir of hematopoietic stem cells but a repository of immunological memory cells. Further characterizing BM-resident memory T cells would be helpful to reveal the complicated relationship between the BM and immunological memory. In this study, we identified CD122high stem cell antigen-1 (Sca-1) high B cell lymphoma 2 (Bcl-2) high CD4+ stem cell-like memory T cells (TSCMs) as a distinct memory T cell subset, which preferentially reside in the BM, where they respond vigorously to blood-borne antigens. Interestingly, the natural CD4+ TSCMs homing to the BM colocalized with VCAM-1+ IL-15+ IL-7+ CXCL-12+ stromal cells. Furthermore, compared to spleen-resident CD4+ TSCMs, BM-resident TSCMs induced the production of high-affinity antibodies against influenza by B lymphocytes more efficiently. Taken together, these observations indicate that the BM provides an appropriate microenvironment for the survival of CD4+ TSCMs, which broadens our knowledge regarding the memory maintenance of antigen-specific CD4+ T lymphocytes.
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Muthuswamy, Ravikumar, AJ Robert McGray, Sebastiano Battaglia, Wenjun He, Anthony Miliotto, Cheryl Eppolito, Junko Matsuzaki, et al. "CXCR6 by increasing retention of memory CD8+ T cells in the ovarian tumor microenvironment promotes immunosurveillance and control of ovarian cancer." Journal for ImmunoTherapy of Cancer 9, no. 10 (October 2021): e003329. http://dx.doi.org/10.1136/jitc-2021-003329.

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PurposeResident memory CD8 T cells, owing to their ability to reside and persist in peripheral tissues, impart adaptive sentinel activity and amplify local immune response, and have beneficial implications for tumor surveillance and control. The current study aimed to clarify the less known chemotactic mechanisms that govern the localization, retention, and residency of memory CD8 T cells in the ovarian tumor microenvironment.Experimental designRNA and protein expressions of chemokine receptors in CD8+ resident memory T cells in human ovarian tumor-infiltrating CD8+ T cells and their association with survival were analyzed. The role of CXCR6 on antitumor T cells was investigated using prophylactic vaccine models in murine ovarian cancer.ResultsChemokine receptor profiling of CD8+CD103+ resident memory tumor-infiltrating lymphocytes in patients with ovarian cancer revealed high expression of CXCR6. Analysis of The Cancer Genome Atlas (TCGA) (ovarian cancer database revealed CXCR6 to be associated with CD103 and increased patient survival. Functional studies in mouse models of ovarian cancer revealed that CXCR6 is a marker of resident, but not circulatory, tumor-specific memory CD8+ T cells. CXCR6-deficient tumor-specific CD8+ T cells showed reduced retention in tumor tissues, leading to diminished resident memory responses and poor control of ovarian cancer.ConclusionsCXCR6, by promoting retention in tumor tissues, serves a critical role in resident memory T cell-mediated immunosurveillance and control of ovarian cancer. Future studies warrant exploiting CXCR6 to promote resident memory responses in cancers.
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Paik, Daniel H., and Donna L. Farber. "Lung tissue resident memory T cells coordinate effector T cell dynamics during the protective recall response to influenza." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 173.7. http://dx.doi.org/10.4049/jimmunol.200.supp.173.7.

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Abstract Influenza remains a serious public health challenge as the current vaccination strategy cannot protect against new strains that emerge every season. Tissue resident memory T cells (TRM) are a non-circulating memory subset that are generated in the lung after influenza infection or intranasal live vaccination, and these lung TRM have been shown to confer broad cross-strain protection. However, the mechanisms by which both CD4+ and CD8+ TRM mediate their protective response are not well defined. We investigated the tissue specific events during an active murine influenza response, including TRM-mediated protection and effector T cell trafficking. To specifically determine the role of TRM, we treated mice with the drug Fingolimod (FTY720), which sequesters circulating lymphocytes into secondary lymphoid organs, enriching the lung for tissue resident memory cells. We found that TRM immediately confer protection, with reduced viral titers evident as early as day 3 after infection. At later time points beginning at days 4–5 post infection, we determined that CD4+ and CD8+ TRM enhance the recruitment of influenza-specific effector T cells into the lung resident niche as well as CD4+ and CD8+ lymphocyte in situ proliferation as measured by BrdU incorporation. Furthermore, total lung RNA sequencing during active infection and FTY720 treatment reveal candidate TRM-associated chemokine pathways for tissue lymphocyte trafficking. These findings indicate that TRM uniquely influence the cellular dynamics of the lung resident niche to mediate cross-strain protection against influenza.
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Goldrath, Ananda. "Transcriptional Control of Memory T Cell Differentiation." Blood 132, Supplement 1 (November 29, 2018): SCI—7—SCI—7. http://dx.doi.org/10.1182/blood-2018-99-109536.

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Abstract Tissue-resident memory CD8+ T cells (TRM) are optimally positioned at common sites of pathogen exposure, where they elicit rapid and robust antiviral immune responses. However, the molecular signals controlling tissue residency and homeostasis of TRM remain unclear. Exploiting a dual-screening platform integrating computational and RNAi in vivo screening approaches, we have identified transcriptional regulators of TRM differentiation. This strategy revealed numerous transcription factors with indispensable roles in TRM differentiation and homeostasis. Further, we show that tumor infiltrating lymphocytes (TIL) share a core TRM transcriptional signature, and that these factors control TIL residency. These results provide novel insight into the biology of T cell residency, which could be leveraged to enhance vaccine efficacy or adoptive therapy treatments against cancer. Disclosures No relevant conflicts of interest to declare.
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Dong, J. "Human bone marrow-resident and blood-circulating memory T lymphocytes." Zeitschrift für Rheumatologie 77, no. 5 (May 25, 2018): 409–11. http://dx.doi.org/10.1007/s00393-018-0485-7.

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Mami-Chouaib, Fathia, Isabelle Tihy, and Stephanie Corgnac. "Resident memory T cells in antitumor immunity and cancer immunotherapy." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 63.06. http://dx.doi.org/10.4049/jimmunol.208.supp.63.06.

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Abstract Tumor-resident memory T (TRM) cells play an important role in cancer diseases. Accumulating evidence indicates that subpopulations of CD3+CD8+ tumor-infiltrating lymphocytes (TIL) are TRM cells, and are emerging as activated tumor-specific T cells. These TRM are characterized by expression of CD103 integrin and identify tumor-reactive cytotoxic T lymphocytes. Human lung tumor CD103+CD8+ TRM co-express CD49a and CD69, and are associated with a favorable prognosis. They also express a panel of T-cell inhibitory receptors, including PD-1, and are able to kill autologous tumor cells upon blockade of PD-1 with neutralizing antibodies. This CD103+CD8+ TRM subset also emerges as a predictive biomarker of response to PD-1 blockade and expands during anti-PD-1 treatment in responder, but not in non-responder patients. It is now widely admitted that expression of CD103 on activated CD8+ T lymphocytes and persistence of TRM in epithelial tissues requires TGF-β. This cytokine is secreted in the tumor microenvironment in its inactive form bound to latency-associated protein, and is activated by αV integrins on tumor cells and immune cells. Using multiplex immunofluorescence staining on cohorts of anti-PD-(L)1-treated lung cancer patients, we recently showed that decreased expression of tumor αV is associated with improved immunotherapy-related-progression-free survival and correlates with an increased density of CD8+CD103+ TIL. Cancer cell αV activates autocrine TGF-β and participates in inducing CD103 on activated CD8+ T cells. Our more recent studies in mouse tumor models and human cancers demonstrate that different CD8+ TRM subsets participate to response different immune checkpoint inhibitors and therapeutic cancer vaccines. Supported by ARC, INCa, Ligue Supported by ARC, INCa, Ligue
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Siracusa, Francesco, Pawel Durek, Mairi A. McGrath, Özen Sercan‐Alp, Anna Rao, Weijie Du, Carla Cendón, et al. "CD69 + memory T lymphocytes of the bone marrow and spleen express the signature transcripts of tissue‐resident memory T lymphocytes." European Journal of Immunology 49, no. 6 (January 30, 2019): 966–68. http://dx.doi.org/10.1002/eji.201847982.

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Bachnak, Louay, Matthew Godwin, and James B. McLachlan. "Assessing how biological sex effects tissue-resident memory T cell responses to influenza infection." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 182.06. http://dx.doi.org/10.4049/jimmunol.208.supp.182.06.

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Abstract The severity and outcome of influenza virus infection are dependent on various host factors including sex. During the 1918 influenza pandemic, males succumbed to viral infections more than females. Following seasonal influenza vaccination, haemagglutination inhibition titers are significantly higher in females than males. Additionally, the Tlr7 gene that recognizes influenza viruses is located on the X chromosome, resulting in higher expression in females. It is not known whether sex influences non-lymphoid tissue residency of lymphocytes during influenza infection. To explore this, we infected male and female mice intratracheally with 20 PFU influenza virus (A/PR8/H1N1). No significant change was noted in weight loss; however, females displayed a higher survival rate and milder clinical disease nine days post-infection. Lungs of female mice contained greater numbers of influenza-specific tissue-resident CD4+ T-cells compared to males. To assess the role of extra-lymphoid tissues in tissue residency in both sexes, we infected male and female lymphotoxin-a knockout (LTa KO) splenectomized mice that resulted in a total lack of all lymphoid tissues. Physiological differences trended the same for both males and females, with no significant weight difference; however, LTa KO females generated more tissue-resident CD4+ T-cells, while males displayed greater numbers of tissue-resident CD8+ T-cells. Overall, females generated a stronger immune response in the absence of lymphoid tissues in response to the virus. Taken together, our data reveal a novel sex-based effect of viral infection on tissue-resident lymphocytes and non-lymphoid tissue immunity. Supported by a grant from the W.M. Keck Foundation
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Dissertations / Theses on the topic "Resident memory T lymphocytes"

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Gamradt, Pia. "Tissue-resident memory T cells in eczema : contribution and protective regulatory mechanisms." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1306/document.

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Les eczémas [eczéma allergique de contact (EAC) et l'eczéma atopique (EA)] sont des dermatoses inflammatoires fréquentes des pays industrialisés. Elles sont induites suite au recrutement et à l'activation dans la peau de lymphocytes T spécifiques d'allergènes, qui sont présents dans notre environnement, et qui sont habituellement très bien tolérés par la majoritédes individus exposés. Ce travail de thèse porte sur un aspect novateur de la physiopathologie des eczémas, à savoir : la contribution des lymphocytes T mémoires résidants (LTrm) dans la peau à la chronicité et à la sévérité de ces maladies.Capitalisant sur des modèles précliniques pertinents ainsi que sur des échantillons cliniques prélevés chez les patients, ce travail a permis d'acquérir de nouvelles connaissances : (i) de nombreux LTrm CD8+ spécifiques colonisent les lésions d'eczéma (ii) ils s'accumulent avecla persistance de l'allergène dans la peau, (iii) ils jouent un rôle majeur dans les récidives de la maladie, mais (iv) ils expriment à leur surface divers récepteurs inhibiteurs, tels que PD-1 ou TIM-3, qui empêchent la survenue de réponses allergiques excessives.Ces travaux apportent donc des informations majeures sur la nature unique des LTrm CD8+ spécifiques d'allergènes et des mécanismes qui contrôlent leur réactivation, afin de préserver l'intégrité de la peau et la survenue de réactions chroniques sévères. Le développement des nouvelles stratégies thérapeutiques ciblant la réactivation des LTrm via leurs récepteursinhibiteurs pourrait permettre de restaurer la tolérance chez les individus allergiques
Allergic contact dermatitis (ACD) and atopic dermatitis (AD), also referred to contact or atopic eczema, are frequent skin inflammatory diseases with increasing prevalence and high socioeconomic impact in Western countries. Eczemas are the prototype of skin delayed-type hypersensitivity reactions. Skin lesions are induced by the recruitment and activation in the skin of effector/memory T cells specific for environmental antigens that are innocuous to healthy non-allergic individuals.The aim of this work was to better understand the pathophysiology of eczemas by a comprehensive analysis of the contribution of skin resident memory T cells (Trm) to the chronicity and severity of these diseases.Capitalizing on relevant preclinical eczema models and on clinical samples collected from allergic patients, this work showed that: (i) numerous allergen-specific CD8+Trm colonize the eczema lesion, (ii) they accumulate in the epidermis in response to the long-term persistence of the allergen in the skin, (iii) they are instrumental for the recurrence of eczema, but (iv) theyexpress several inhibitory check point receptors (ICRs, such as PD-1, TIM-3) at their surface, which keep them in check to prevent the development of severe immunopathology.Thus, our work provides important information for considering the unique nature of hapteninduced CD8+ Trm and the mechanisms that prevent their unwanted reactivation and subsequent development of chronic or severe skin allergy. The development of therapeutic strategies targeting the reactivation of skin Trm in situ via their ICRs should open new avenues to restore tolerance in allergic individuals
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Malenica, Ines. "Role of Tissue-Resident Memory T (TRM) Cells in CD8+ T Cell Immunity and Response to Anti-PD-1 Immunotherapy : Involvement of TGF-β and αV Integrins." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS201.

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La survie des patients atteints de cancer et traités avec des thérapies conventionnelles reste faible dans plusieurs types de tumeurs. Récemment, une nouvelle approche immunothérapeutique a été développée pour cibler le système immunitaire au lieu de la tumeur elle-même, afin de restaurer la fonctionnalité des cellules immunitaires et la destruction des cellules cancéreuses. L’immunothérapie ciblant le récepteur inhibiteur PD-1 occupe une place privilégiée dans les thérapies anticancéreuses en raison de sa haute spécificité et de sa faible toxicité par rapport aux thérapies conventionnelles. Cependant, le taux de réponse reste faible avec seulement 20 à 25% de patients répondant à une immunothérapie anti-PD-1. Il est donc important de comprendre les mécanismes associés à la résistance à ces thérapies et d’identifier des biomarqueurs prédictifs de réponse. L'expression du ligand de PD-1, PD-L1, sur les cellules tumorales, la charge mutationnelle tumorale et l'infiltration tumorale par les lymphocytes ont déjà été décrits, mais de nouveaux biomarqueurs sont nécessaires pour mieux déterminer la sous-population de patients susceptible de bénéficier de ces traitements. Au cours de ce travail, nous avons établi une cohorte de 118 patients atteints d'un cancer du poumon non à petites cellules (CBNPC) traités avec une immunothérapie anti-PD-1/PD-L1, et nous avons étudié l'expression de plusieurs biomarqueurs potentiels, en particulier les cellules T mémoires résidentes dans le tissu (TRM) CD8+CD103+. Ces cellules constituent un candidat potentiel car elles représentent une population privilégiée de lymphocytes T CD8 grâce à l’expression de PD-1 et une forte capacité cytotoxique vis-à-vis des cellules tumorales autologues suite à la neutralisation de l’interaction de PD-1 avec PD-L1. Nous montrons qu’une forte infiltration de tumeurs de CBNPC avec des cellules TRM corrèle à une survie sans progression plus élevée (PFS) et une réponse plus efficace à anti-PD-1 que les tumeurs avec une faible infiltration par des TRM. De plus, les tumeurs qui expriment fortement ICAM-1, un ligand de l’intégrine LFA-1 exprimée sur les lymphocytes T CD8, sont hautement infiltrées par des TRM. Par ailleurs, il est bien connu que le signal TGF-β est crucial pour l’induction de CD103 et la formation de TRM CD8+CD103+. Je me suis donc intéressée à l'activation du TGF-β par les intégrines αV exprimée par les cellules tumorales humaines et murines. À l'aide des modèles in vitro et in vivo, nous montrons que les cellules tumorales exprimant les intégrines αV activent le TGF-β et induisent l'expression de CD103 à la fois par les cellules T CD8+ provenant de cellules mononucléées du sang périphérique (PBMC) et de lymphocytes infiltrant la tumeur (TIL). L’expression plus faible de CD103 par les TIL CD8+ de souris greffées avec des tumeurs déficientes pour l’expression d'αV n'a pas d'effet sur le contrôle de la croissance tumorale. De manière intéressante, nous montrons dans des modèles de tumeurs déficientes pour l’expression d’αV, que le traitement avec des anticorps anti-PD-1 bloquants corrèle avec un meilleur contrôle de la croissance tumorale et une meilleure réponse à l'immunothérapie anti-PD-1 qui sont associés à une infiltration plus forte de TIL et un état d'activation plus élevé des TIL CD8+ exerçant une activité cytotoxique spécifique. De plus, une expression élevée de l'intégrine αV dans les tumeurs corrèle avec une réponse plus faible des patients atteints de CBNPC à une immunothérapie anti-PD-1/PD-L1. Ces données montrent comment trois marqueurs distincts, cellules TRM, ICAM-1 et les intégrines αV, régulent le microenvironnement tumoral et l’immunité T CD8 avec des implications potentielles pour potentialiser les réponses aux immunothérapies
The survival of cancer patients treated with conventional therapies remains low in multiple cancers. Recently, a new immunotherapeutic approach has been developed to target the immune system instead of the tumor itself, in order to restore immune cell functions in cancer destruction. Immunotherapy targeting the T cell inhibitory receptor PD-1 occupies a privileged place in cancer therapy thanks to its high specificity and low toxicity compared to chemotherapies. However, the response rate remains low with only 20-25% of patients responding to anti-PD-1 immunotherapy. An important issue is therefore to understand the mechanisms associated with resistance to these therapies and to identify the predictive biomarkers of response. The expression of the PD-1 ligand, PD-L1, on tumor cells, tumor mutational burden (TMB) and tumor infiltration by lymphocytes have been described to predict the response to immune checkpoint blockade (ICB). However, new biomarkers are needed to better determine patient subpopulation which could benefit from this treatment. To address this question, we established a cohort of 118 non-small cell lung cancer (NSCLC) patients treated with anti-PD-1/PD-L1 immunotherapy and studied the expression of several potential biomarkers. Tissue-resident memory T (TRM) cells are a potential candidate because they represent a distinct population of CD8+ T cells highly expressing integrin αEβ7 (CD103) and PD-1; and showing strong cytotoxic capacity towards autologous tumor cells upon neutralisation of PD-1/PD-L1 interaction. Results from the present study show that high infiltration of TRM cells in NSCLC tumors correlates with higher progression-free survival (PFS) and a better response to anti-PD-1/PD-L1 immunotherapy. Moreover, tumors with high expression levels of ICAM-1, the ligand of integrin LFA-1 expressed on T cells, show higher TRM infiltration. TGF-β is a cytokine directly involved in CD103 induction on activated tumor-specific T cells. Therefore, I also investigated the role of αV integrins in activating TGF-β and thereby in controlling TRM differentiation and anti-tumor T cell immunity. Using human and mouse models, we show that tumor cells expressing αV integrins activate TGF-β, which can in turn induce expression of CD103 on CD8+ T cells in vitro on peripheral blood mononuclear cells (PBMCs) and in vivo on tumor infiltrating lymphocytes (TIL). However, lower CD103 expression on CD8+ TIL and thus CD103+ TRM cell formation in C57BL/6 mice engrafted with αV-lacking cancer cells had no effect on tumor growth control. Remarkably, αV-deficient tumors responded more effectively to anti-PD-1 immunotherapy than αV-efficient tumors and this response correlates with higher tumor infiltration by activated CD8+ T cells and stronger cytotoxic activity toward autologous cancer cells. Moreover, high expression of αV integrins in NSCLC tumors correlates with worse response to anti-PD-1/PD-L1 immunotherapy. These data show how three distinct markers, TRM cells, ICAM-1, and αV integrins regulate the tumor microenvironment and CD8+ T cell immunity, with potential implications in improving response to ICB immunotherapies
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Bottois, Hugo. "Acquisition and regulation of effector T cell functions in Crohn’s disease." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCC012.

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L’intestin représente un microenvironnement complexe notamment par la présence du microbiote intestinal nécessitant un système immunitaire spécialisé incluant les cellules CD8 T résidente (Trm). Notre but est d’étudier la différentiation et la fonction de ces Trm dans la muqueuse intestinale. Nous souhaitons également identifier l’implication des Trm dans la maladie de Crohn (MC).Des cellules T provenant de sang ont été exposées in vitro dans conditions proches de la muqueuse pour étudier leur différentiation en Trm. L’environnement intestinal est capable de convertir des T CD8 du sang en un phénotype proche de celui de la muqueuse, notamment par l’acquisition de l’intégrine CD103. L'expression mutuellement exclusive de CD103 et KLRG1 sur les CD8 Trm semble définir des sous-populations fonctionnellement distinctes.Les Trm de patients ont été restimulé pour analyser leurs fonctions. Les CD103+ Trm sont plus sensibles à une restimulation TCR, mais les KLRG1+CD8 Trm expriment le Granzyme B sont augmentés dans la muqueuse des patients. Le transcriptome des CD103+ CD8 Trm est considérablement modifié dans la MC et montre une expression de gène associés à des signaux de danger, de réparation tissulaire et de recrutement lymphocytaire comparé aux individus contrôles. En parallèle, Nous avons établi un modèle de coculture d’organoide et de cellules T autologues. Notre but est d'étudier l’interaction et l'effet des ces cellules T sur des cellules épithéliales et de tester l’efficacité des biothérapies ciblant ces interactions comme des anticorps bloquant CD103 ou NKG2D, dont le développement est en cours dans la MC
The intestine is a complex microenvironment that requires an immune system with specific features to maintain homeostasis. Tissue resident memory (Trm) CD8 T cells from the intestinal tissue participate to this regulation. We aimed to study the differentiation and function of human CD8 Trm cells in the intestinal mucosa and their impact on inflammatory disorders such as Crohn’s disease (CD). We tested in vitro the acquisition of a mucosa-associated phenotype, by exposing blood T cells to cytokines mimicking the intestinal microenvironment. This stimulation converted activated blood CD8 T cells to a mucosal-like phenotype, mainly by acquisition of the tissue resident marker, integrin CD103.Blood and mucosal CD8 T cells isolated from CD patients and controls were characterized by flow cytometry to determine the specificities of intestinal Trm cells. Interestingly, the expression of KLRG1 and CD103, both receptor of E-cadherin expressed by epithelial cells, was mutually exclusive. Restimulated Trm cells in vitro showed that CD103 CD8 Trm cells were more responsive to TCR stimulation, while KLRG1 CD8 T cells displayed higher expression of cytotoxic molecules such as granzyme B. These results suggest that these markers define distinct functional Trm subsets.We analysed the transcriptome of sorted Trm subsets from inflammatory or control tissues and showed that CD8 Trm cells expressing CD103 had increase expression of cytokines and chemokines compared to other Trm cells. Additionally, CD103 expressing Trm cells from CD patients showed major transcriptomic differences compared to controls, with increase expression of genes involved in tissue repair and recruitment of immune effector cells. Taken together, these results suggest that Trm cells in the intestine are heterogeneous, as CD103 expressing cells display functions associated with alarm signals and tissue repair, while KLRG1 positive cells exhibit cytotoxic potential. To study the interactions of these T cells with intestinal epithelial cells, we have established intestinal epithelial organoid cultures with mucosal T cells. Our aims are to examine the molecules involved in lympho-epithelial interactions and study their functional consequences. To this end we will test and study the mechanisms of action of blocking antibodies targeting CD103 and NKG2D that are two pathways tested for the treatment of CD
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Blanc, Charlotte. "Lymphocytes T résidents mémoires dans les tumeurs du poumon et ORL : sous-populations et mécanismes de migration Cxcr6-deficiency impairs cancer vaccine efficacy and resident memory CD8+ T cells recruitment in tumor Phénotype et localisation des sous-populations de LT résidents mémoires dans les tumeurs pulmonaires." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCB046.

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De grands bouleversements sont apparus au début du 21ème siècle dans la compréhension de la physiopathologie du cancer avec l'énoncé de la théorie de l'immunoédition complétant le concept de l'immunosurveillance. La communauté scientifique s'accorde désormais sur le fait que le système immunitaire et particulièrement les lymphocytes T (LT) CD8+ tiennent une place essentielle dans le contrôle de la croissance tumorale. Toutefois, par pression de sélection, la cellule tumorale développe des mécanismes de résistance aux attaques du système immunitaire, neutralisant ainsi l'effet cytotoxique des LT. Restaurer leurs fonctions antitumorales est une stratégie thérapeutique qui a fait ses preuves avec l'immunothérapie. Cependant, ces traitements ne sont pas toujours efficaces et peuvent être optimisés par une meilleure compréhension de l'immunité antitumorale. Dans ce but, nous nous sommes intéressés au déroulement de la réponse antitumorale des LT CD8+ en nous attardant sur les LT résidents mémoires (Trm) particulièrement efficaces contre la tumeur et au fort impact pronostic, qui pourrait être une cible thérapeutique pertinente. L'induction d'une réponse antitumorale efficace requière une présentation antigénique optimale conduisant à l'activation du LT CD8+ et à sa migration dans la tumeur via le réseau chimiokine/récepteur. Dans le premier travail, le récepteur de chimiokine CXCR6 a été identifié comme molécule de homing fortement exprimée par les LT CD8+ Trm du poumon. Sa chimiokine CXCL16 peut être sécrétée par les cellules présentatrices d'antigènes, les cellules épithéliales et tumorales mais le rôle de l'axe CXCR6/CXCL16 dans l'immunosurveillance des cancers n'est pas connu à ce jour. Pour en comprendre les mécanismes, des expériences de vaccinations antitumorales par voie intranasale (i.n.) réalisées dans des modèles de souris déficientes en CXCR6 ont permis de mettre en évidence l'impact de CXCR6 dans l'établissement d'une infiltration optimale en LT CD8+ spécifiques et Trm dans le lavage broncho-alvéolaire et au sein des tumeurs des voies aérodigestives supérieures. L'axe CXCR6/CXCL16 pourrait représenter un outil thérapeutique intéressant pour les vaccins anticancéreux ou pour les thérapies de transferts adoptifs de LT modifiés dont l'infiltration intra-tumorale est limitée. Les Trm ont la particularité d'exprimer des intégrines (CD103, CD49a) impliquées dans leur interaction avec le microenvironnement tumoral. Ils présentent un phénotype original microenvironnement-dépendant qui leur confère des avantages en termes d'activités cytotoxiques dans les tumeurs et expliquant leur impact pronostic favorable. Une meilleure connaissance de leur phénotype et de leurs mécanismes d'induction permettrait d'optimiser la réponse antitumorale. Le travail 2 s'est concentré sur l'étude de deux intégrines principales CD103 et CD49a dans les cancers pulmonaires par des techniques multiparamétriques d'immunofluorescence in situ et de cytométrie en flux. Les résultats montrent que leur expression expliquait l'infiltration des LT CD8+ et leur contact avec la cellule tumorale, en lien avec leur forte implication dans la survie des malades. Nos données suggérèrent également la possibilité d'un priming local pulmonaire nécessaire à l'induction du phénotype Trm par des modèles de vaccinations i.n. et d'un lien entre les structures lymphoïdes tertiaires et les Trm. Ces travaux ont montré l'importance de l'analyse de l'immunité locale avec les LT CD8+ Trm pour la compréhension de cette réponse antitumorale. Etudier le phénotype Trm a permis de mettre en lumière leur rôle crucial et leur potentiel comme cible thérapeutique. Une meilleure connaissance des mécanismes sous-jacents à l'induction des Trm permettra à terme de les cibler pharmacologiquement pour optimiser les thérapies et donc la survie des malades
With the immunoediting theory, new concept in the cancer physiopathology has appeared in the beginning of the 21st century. It is now established that the immune system and CD8+ T cells play a crucial role in tumor growth control. However, by selective pressure, the tumor cell develops mechanisms to avoid immune destruction and to inhibit T cells cytotoxicity. Reinvigorating antitumor functions is a well-proven therapeutic strategy with immunotherapy. Nevertheless, patients do not always respond to these treatments which could be optimized. In this context, we had studied antitumor response induction by focusing on CD8+ T cells and especially on resident memory T cells (Trm), new cytotoxic cells correlated with a good prognosis and which could be a relevant therapeutic target. A potent antitumor response requires an optimal antigenic presentation to prime CD8+ T cells and favor their migration into the tumor through chemokine network. In a first study, we identified a chemokine receptor CXCR6, highly expressed by lung CD8+ Trm. Its chemokine CXCL16 is produced by antigen presenting cells, epithelial and tumor cells, but the role of the CXCR6/CXCL16 axis in cancer immunosurveillance is not known yet. To understand its mechanisms, antitumor vaccinations strategies by intranasal (i.n.) route had been set up in CXCR6-deficient mice and had shown the role of CXCR6 in promoting the infiltration of specific CD8+ T cells and Trm in lung tissue and head and neck tumors. The CXCR6/CXCL16 axis could represent an interesting therapeutic tool for antitumor vaccines or adoptive cell transfer in which tumor infiltration is a challenge. Trm have the particularity to express integrins (CD103, CD49a) involved in the interaction with the tumor microenvironment. They exhibit an original and an heterogenous phenotype, microenvironment-dependent. Their phenotype is involved in their cytotoxic activities, highlighting their high prognostic impact and their potential to be a suitable therapeutic target. Better understanding Trm phenotype complexity and their induction mechanisms are crucial to further optimize antitumor response. The second work of this thesis focused on the expression of two main integrins CD103 and CD49a in lung cancer by an in situ multiparametric immunofluorescence technique and by flow cytometry. The results showed that their expression determine their contact with the tumor cells and their involvement in patient survival. Our data obtained by i.n. vaccination models and by tertiary lymphoid structures analysis suggest the possibility of a priming in the lung to induce the Trm phenotype. Our work shows the necessity of analyzing local immunity and CD8+ Trm T cells for a better understanding of antitumor response. Studying Trm phenotype has highlighted their crucial role and their potential to be a relevant therapeutic target. Identifying and targeting their mechanisms of induction might optimize therapies and patient's survival
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Koo, Yoon. "The impact of pertussis toxin on T cell functions." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0077.

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La toxine pertussique (PTX) est une exotoxine produite uniquement par Bordetella pertussis, un pathogène de la coqueluche. Les effets de la toxine au cours d'une infection bactérienne sont bien connus, et sont pour la plupart liés à son activité ADP-ribosyltransférase qui cible les GPCRs. Or, la PTX est un antigène majeur permettant d’établir une réponse immunitaire contre B. pertussis ce qui en fait donc un composant principal de tous les vaccins anti-coqueluche actuels. De nombreux travaux sur la PTX concernent ses mécanismes moléculaires et son rôle durant la phase d'infection. Mais, il y a un manque d'information sur le rôle immunogène de la PTX.En utilisant un modèle d'infection intranasale par B. pertussis, nous avons constaté que la génération de lymphocytes T CD4 mémoires résidant (Trm) dans les poumons dépendait de l'exposition à la PTX. La toxine pertussique est couramment utilisée pour inhiber la réponse aux chimiokines, dans l'étude de la migration des cellules T. Etant donné que la plupart des récepteurs aux chimiokines sont des GPCRs, la mobilité de nombreuses cellules immunitaires, y compris les cellules T, est facilement affectée par la PTX. La migration des cellules T est un phénomène sophistiqué régulé spatio-temporellement. Nos résultats démontrent que la PTX n’affecte pas les étapes de la migration dépendantes des intégrines lorsque les cellules T sont activées.Ce travail s’intéresse à l'impact de la PTX sur la biologie des cellules T en étudiant son rôle dans la réponse immunitaire adaptative in vivo, dans un modèle animal d'infection et son impact sur la migration des lymphocytes T in vitro
Pertussis toxin (PTX) is an exotoxin uniquely produced from Bordetella pertussis, a human respiratory tract pathogen causing pertussis disease, also known as whooping cough. The toxin is well described its virulence effects during bacterial infection. Most of these effects are due to ADP-ribosyltransferase activity of the molecule that targets G-protein coupled receptors (GPCR). On the other hand, PTX is an important antigen that provides protection against pertussis disease and a major component of all current pertussis vaccines. There are numerous literatures on PTX about its molecular mechanisms and its role during infection phase. Instead, lack of information on how PTX contributes host’s adaptive immunity has incurred confusion in understanding the immunogenic role of PTX. With intranasal infection model of B. pertussis, we detected the generation of CD4 lung-resident memory T cells (Trm) were depending on PTX exposure. For T cell migration study, PTX is being used to inhibit chemokine response. Because most of chemokine receptors are GPCR, the motility of many immune cells including T cells is easily affected by PTX. T cell migration is a sophisticate phenomenon regulated space-temporally. The results demonstrated, once T cells become activated and effector, are less influenced than inactivated T cells.This thesis reports the impact of PTX on T cells in two parts; 1) Role of PTX in adaptive immune response by in vivo infection system and 2) Influence of PTX on T cell motility by in vitro assays
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Dal, Cin Julian. "Analyse tissulaire des myopathies inflammatoires idiopathiques et induites par immune-checkpoint-inhibitor : apport des nouvelles approches transcriptomiques." Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS151.pdf.

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Les myosites forment un groupe hétérogène de pathologies auto-immunes partageant une atteinte musculaire des patients. Les myosites sont séparées en 5 sous-entités : les dermatomyosites (DM), les syndromes des anti-synthétases (ASyS), les myosites à inclusions (IBM), les myopathies nécrosantes auto-immunes (IMNM) et les myosites induites par inhibiteur de point de contrôle immunitaire (ICI). Les mécanismes physiopathologiques, le phénotype clinique et le pronostic de chaque sous-entité sont différents. Parmi les myosites, ce travail s’est concentré sur les IMNM et les myosites induites par ICI, leur pronostic étant le plus sombre. Des études transcriptomiques à haute résolution, spatiale ainsi qu’en cellule unique ont permis d’étudier le tissu musculaire des patients atteints de ces myosites. Dans les myosites induites par ICI, ces études ont confirmé la cytotoxicité de lymphocytes T CD8 et leur rôle central, principalement celui des populations de lymphocytes T résidents mémoires identifiés dans le muscle ainsi que des macrophages. Nous proposons un modèle pathogénique basé sur la réaction de lymphocytes T résidents mémoires aux traitements ICI. Dans les IMNM, des sous-groupes de macrophages ont été identifiés composés respectivement des macrophages pro-inflammatoires, anti-inflammatoires et de macrophages accompagnés de progéniteurs fibro-adipeux (FAP). Nous proposons que la nécrose stimulerait les macrophages et induirait leur recrutement ce qui permettrait la prolifération des FAP à l’origine de la fibrose exacerbée des patients. La compréhension de ces mécanismes parmi d’autres permet d’envisager de nouvelles cibles thérapeutiques et d’améliorer le pronostic des patients
Myositis are a heterogeneous group of autoimmune pathologies characterized by muscle damage in patients. Myositis are separated into 5 subgroups: dermatomyositis (DM), anti-synthetase syndromes (ASyS), inclusion body myositis (IBM), autoimmune necrotizing myopathies (IMNM) and immune-checkpoint inhibitor (ICI)-induced myositis. The pathophysiological mechanisms, clinical phenotype and prognosis of each subgroup are different. Among myositis, this work focused on IMNM and ICI-induced myositis, which have the poorest prognosis. High-resolution, spatial and single-cell transcriptomic studies have made it possible to study the muscle tissue of patients with these myositis. In ICI-induced myositis, these studies have confirmed the cytotoxicity of CD8 T cells and their central role, mainly of a population of resident memory T cells identified in the muscle, as well as macrophages. We propose a pathogenic model based on the reaction of resident memory T cells to ICI treatments. In IMNM, subgroups of macrophages have been identified composed respectively of pro-inflammatory macrophages, anti-inflammatory macrophages, and macrophages close to fibro-adipogenic progenitors (FAP). We propose that necrosis can stimulate macrophages and induce their recruitment, which would allow the proliferation of FAPs at the origin of exacerbated fibrosis in patients. Understanding mechanisms among others makes it possible to consider new therapeutic targets and improve patient prognosis
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Bell, James Jeremiah. "T cells from immunological memory to autoimmune disease." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/5885.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2006.
Title from title screen of research.pdf file (viewed December 22, 2006). The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2006" Includes bibliographical references.
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Woyciechowski, Sandra [Verfasser], and Hanspeter [Akademischer Betreuer] Pircher. "Regulation of tissue-resident memory CD8+ T cells in salivary glands." Freiburg : Universität, 2018. http://d-nb.info/1196526257/34.

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Cendón, Carla. "Function and compartmentalization of circulating versus tissue resident memory T cells." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/19794.

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Verstärkte Anstrengungen zur Förderung der T-Zell-basierten Immunität haben eine zwingende Notwendigkeit für unser Verständnis der menschlichen T-Zell-Funktion und –Erhaltung geschaffen. Das Paradigma, dass Gedächtnis-T-Lymphozyten kontinuierlich durch den Körper zirkulieren wurde vor kurzem durch die Entdeckung der Gedächtnis-T-Zellen, die in einer Vielzahl von Geweben, einschließlich des Knochenmarks angesiedelt sind, herausgefordert. Allerdings bleibt der Unterschied zwischen Funktionsweise von zirkulierenden und gewebeansässigen Gedächtnis-T-Zellen nur unzulänglich verstanden. Die Knochenmark ist die Heimat für eine große Anzahl Gedächtnis-T-Zellen. CD4+ Gedächtnis-T-Zellen aus dem Knochenmark beinhalten ein breites Spektrum an Antigenspezifitäten. Interessanterweise wurden CD4+ Gedächtnis-T-Zellen spezifisch für systemische Kindheitsantigene im Knochenmark von älteren Menschen gefunden, auch wenn sie nicht mehr in der Blutzirkulation nachgewiesen werden konnten. Gedächtnis-T-Zellen aus dem Knochenmark sind sesshaft und ruhend und Langzeitgedächtnis gegen systemische Antigene erhalten. Sowohl der Überlebensmechanismus von Gedächtnis-T-Zellen, als auch die Kapazität von gewebsansässigen Gedächtnis-T-Zellen nach einer systemischen Herausforderung mobilisiert zu werden, sind bisher nur unzureichend geklärt. Ich habe gezeigt, dass Gedächtnis-T-Zellen aus dem peripheren Blut und Knochenmark unterschiedliche Überlebensfähigkeiten haben. Weiterhin habe ich die Rolle von Überleben Faktoren in ihrer Erhaltung identifiziert. Zudem habe ich bestimmt, dass Gedächtnis-T-Zellen aus dem Blut und Knochenmark unterschiedliche Zellpopulationen sind, mit unterschiedliche TCRβ Repertoires. Schließlich konnte ich zeigen, dass sesshafte Gedächtnis-T-Zellen, die spezifisch für systemische Antigene sind, schnell in die Blutzirkulation mobilisiert werden. Zusammenfassend bieten diese Studien ein umfassenderes Verständnis der Funktion und des Erhalts des immunologischen Gedächtnisses.
Intensified efforts to promote protective T cell-based immunity in vaccines and immunotherapies have created a compelling need to expand our understanding of human T cell function and maintenance. The paradigm that memory T lymphocytes are continuously circulating through the body in search of their cognate antigen has been recently challenged by the discovery of memory T cells residing in a variety of tissues, including the bone marrow (BM). However, the division of labor and lifestyle of circulating versus tissue resident memory T cells remains poorly understood. The human BM is home to a great number of memory T cells. BM memory CD4+ T cells contain a wide array of antigen specificities. Interestingly, memory CD4+ T cells specific for systemic childhood antigens have been found in the BM of elderly humans, even when they were no longer detectable in peripheral blood (PB) circulation. BM memory T cells are resident, resting and maintain long-term memory to systemic antigens. The survival mechanisms of circulating and BM resident memory T cells; as well as the capacities of tissue resident memory T cells to be mobilized into blood circulation after systemic antigen re-challenge to confer us with immune protection remains to be elucidated. I have shown that PB and BM memory T cells have different survival capacities, as well as identified the role of survival factors in their maintenance. Moreover, using sequencing analysis of the TCRβ repertoire, I have determined that PB and BM memory T cells are separated cell populations. Finally, by tracking the dynamics of antigen-specific memory CD4+ T cells after systemic MMR re-vaccination I could show that TRM CD4+ T cells specific for systemic antigens can be rapidly mobilized into blood circulation and contribute to the immune response. These studies provide a more comprehensive understanding of the function and maintenance of immunological memory in humans.
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Winter, Samantha. "The role of tissue-resident memory T cells in cutaneous metastatic melanoma." Thesis, Winter, Samantha (2014) The role of tissue-resident memory T cells in cutaneous metastatic melanoma. Honours thesis, Murdoch University, 2014. https://researchrepository.murdoch.edu.au/id/eprint/32067/.

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Metastatic melanoma is a highly aggressive form of cancer, with poor prognosis when diagnosed during late stages. Modern cancer immunotherapies that exploit the immune system were praised as the science ‘breakthrough of the year’ in 2013 and are exhibiting improved outcomes in the treatment of advanced melanoma. Two of these immunotherapies currently approved for clinical use are known as anti-CTLA-4 and anti-PD-1, which respectively target the cell surface markers CTLA-4 and PD-1 on CD8 T cells. CD8 T cell subsets play a superior role in inflammation and have the ability to destroy cancer cells. Following resolution of inflammation, a small number of CD8 T cells contract to form a stable pool of memory T cells. These memory CD8 T cells have the ability to mount a faster and stronger immune response compared to their short-lived predecessors. Due to their superior function and the immunogenicity of melanoma, these memory CD8 T cells play a pivotal role in the development of successful immunotherapeutic treatments. Recently, a subset of non-migratory memory CD8 T cells that reside at peripheral sites has been described, known as tissue-resident memory T cells (TRM). TRM cells are found primarily at barrier sites, such as the epidermis of the skin. Current research surrounding TRM cells has centred primarily on their role in viral infections. This project explores the presence and phenotype of TRM cells at the site of cutaneous murine melanoma. A novel model of melanoma engraftment was utilised that resembles the human disease with increased accuracy due to epidermal/dermal infiltration, which is not seen in traditional murine melanoma models. TRM cells were able to be identified, enumerated and phenotyped at different stages of tumour control, by designing a protocol which employed cutaneous melanoma, traceable tumour-specific gBT.I CD8 T cells and HSV-1 infection. TRM cells were found to be present at the site of tumour at numbers similar to unmanipulated control skin. In contrast, elevated numbers were seen in HSV-1 infected skin. At the site of cutaneous melanoma, TRM cells were found to have a KLRG1lo, CTLA-4hi and PD-1lo phenotype at each time point analysed, identical to TRM cells isolated from control and HSV-1 infected skin. These findings suggest the need for further research into TRM cell function during immunotherapy, as expression of CTLA-4 and PD-1 surface markers render TRM cells as potential targets for anti-CTLA-4 and anti-PD-1 monoclonal antibody treatment.
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Books on the topic "Resident memory T lymphocytes"

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Zanetti, M. Memory T cells. New York: Springer Science+Business Media, 2010.

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Memory T cells. New York: Springer Science+Business Media, 2010.

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Cvetkovski, Filip. Transcriptional control of tissue-resident memory T cell generation. [New York, N.Y.?]: [publisher not identified], 2019.

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Kumar, Brahma Vencel. Identification and characterization of tissue-resident memory T cells in humans. [New York, N.Y.?]: [publisher not identified], 2018.

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Mami-Chouaib, Fathia, and Eric Tartour, eds. Tissue-Resident Memory T Cells. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-960-5.

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Gray, David. Immunological Memory (Current Topics in Microbiology & Immunology). Edited by David Gray. Springer, 1990.

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Schluns, Kimberly Sue, and Kim Klonowski, eds. Diverse functions of mucosal resident memory T cells. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-539-8.

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Goplen, Nick P., Toshinori Nakayama, Jie Sun, and Shiki Takamura, eds. Resident Memory T Cells: Guardians of the Balance of Local Immunity and Pathology. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-548-0.

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Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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Book chapters on the topic "Resident memory T lymphocytes"

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Iijima, Norifumi. "Memory Lymphocyte Clusters in Genital Immunity: Role of Tissue-Resident Memory T Cells (TRM)." In Current Topics in Microbiology and Immunology, 83–117. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/82_2020_213.

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McLean, Angela R. "Modelling T Cell Memory in Vivo and in Vitro." In T Lymphocytes, 227–34. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_24.

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Lugli, Enrico, Veronica Zanon, Domenico Mavilio, and Alessandra Roberto. "FACS Analysis of Memory T Lymphocytes." In Methods in Molecular Biology, 31–47. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6548-9_3.

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Williams, Jason B., and Thomas S. Kupper. "Resident Memory T Cells in the Tumor Microenvironment." In Advances in Experimental Medicine and Biology, 39–68. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49270-0_3.

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MacDonald, H. R., R. C. Budd, and J. C. Cerottini. "Pgp-1 (Ly 24) As a Marker of Murine Memory T Lymphocytes." In Immunological Memory, 97–109. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75244-5_6.

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Horgan, Kevin J., Yoshiya Tanaka, and Stephen Shaw. "Postthymic Differentiation of CD4 T Lymphocytes: Naive Versus Memory Subsets and Further Specialization among Memory Cells (Part 1 of 2)." In Regulation and Functional Significance of T-Cell Subsets, 72–87. Basel: KARGER, 1992. http://dx.doi.org/10.1159/000319115.

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Horgan, Kevin J., Yoshiya Tanaka, and Stephen Shaw. "Postthymic Differentiation of CD4 T Lymphocytes: Naive Versus Memory Subsets and Further Specialization among Memory Cells (Part 2 of 2)." In Regulation and Functional Significance of T-Cell Subsets, 88–102. Basel: KARGER, 1992. http://dx.doi.org/10.1159/000319116.

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Kannagi, Reiji, Katsuyuki Ohmori, Guo-Yun Chen, Keiko Miyazaki, Mineko Izawa, and Keiichiro Sakuma. "Sialylated and Sulfated Carbohydrate Ligands for Selectins and Siglecs: Involvement in Traffic and Homing of Human Memory T and B Lymphocytes." In Advances in Experimental Medicine and Biology, 549–69. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7877-6_29.

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Jebisha, Dr L., Dr R. Sathish Muthukumar, Dr C. Sreeja, and Dr Merlin Jayaraj. "ROLE OF IMMUNE CELLS IN PERIODONTAL DISEASE." In Emerging Trends in Oral Health Sciences and Dentistry. Technoarete Publishers, 2022. http://dx.doi.org/10.36647/etohsd/2022.01.b1.ch016.

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Periodontitis is intricate & multi-factorial lesion. It is characterized by a group of inflammatory conditions in the periodontium which is caused by bacteria. Chronic inflammation is precise by B and T cells by the initiation in cytokine secretion, then osteoclastogenesis is modulated. The objective of the article briefly reviews the recent research and the consequence in B cell & T lymphocytes subsets, and the expression of cytokine seen in the morbific of the periodontitis. Gingival homeostasis is maintained by T reg (T regulatory), CD8+ T, and tissue-resident γδ, T cells plays a vital role in gingival hemostasis. Clinically healthy periodontium has a low percentage of memory B cells, evade bone damage due to subclinical inflammation. The RANKL -dependent method makes an alveolar bone loss and causes periodontitis. Stimulation of T and B lymphocytes subunits is one that causes either the seditious lesion will alleviate in chronic gingivitis or it may advance to a tissue destructive periodontitis.
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Akbaba, Hasan. "Resident Memory T Cells." In Cells of the Immune System. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.90334.

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Conference papers on the topic "Resident memory T lymphocytes"

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Sanders, N., A. T. Shenoy, D. Y. Chen, D. Bean, M. Sagar, M. Saeed, and J. P. Mizgerd. "OC43 Coronavirus Infections in Mice Elicit Lung Resident Memory T Cells." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3122.

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Rosato, Pamela C., Luke S. Manlove, Christine E. Nelson, Christopher A. Pennell, Vaiva Vezys, and David Masopust. "Abstract B056: Harnessing tissue resident memory T cells to combat solid tumors." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b056.

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Schoettler, N., K. M. Blaine, and A. I. Sperling. "CD4 Tissue Resident Memory T Cell Stimulation Activates Asthma-Relevant Inflammatory Pathways." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1256.

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Mack, Patricia, Manuel Stöth, Joshua Mannal, Till Meyer, Pascal Ickrath, Stephan Hackenberg, and Agmal Scherzad. "Tissue-resident memory CD8 T cells als prognostischer Marker beim sinunasalen Plattenepithelkarzinom." In 95. Jahresversammlung Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e. V., Bonn. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1784150.

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Baranova, Elena, Amanda Finan-Marchi, Manon Motte, Maroua Tliba, Sabine Iglesias, Carole Belda, Alexandra Mace, et al. "Abstract 4988: Multiplex immunofluorescence detection of resident memory T cells in solid tumors." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4988.

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Richmond, Bradley, Ana Serezani, Jacob Schaff, and Timothy Blackwell. "Tissue resident memory T cells are increased in the lungs of COPD patients." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.247.

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Yang, H., and J. K. Kolls. "Single-Cell RNA-seq Revealed T Cell Metabolism as a Target to Tissue-Resident Memory T Cell Contraction." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2603.

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Park, Hye Seon, Young-Ae Kim, Won Seon Bang, Heejae Lee, Miseon Lee, In Ah Park, In Hye Song, et al. "Abstract 4685: Phenotypic difference of CD103+tissue-resident memory T cells in various cancers." 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.am2018-4685.

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Song, Erwei, Yue Xing, and Shicheng Su. "Abstract 1892: Dysfunction of resident memory CD8+T cells facilitates breast cancer lung metastasis." 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.sabcs18-1892.

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Song, Erwei, Yue Xing, and Shicheng Su. "Abstract 1892: Dysfunction of resident memory CD8+T cells facilitates breast cancer lung metastasis." 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.am2019-1892.

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