Bibliographies thématiques / Type 1 regulatory T (Tr1) cells, Cytotoxicity, Immune regulation, granzyme B

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Littérature scientifique sur le sujet « Type 1 regulatory T (Tr1) cells, Cytotoxicity, Immune regulation, granzyme B »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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Articles de revues sur le sujet "Type 1 regulatory T (Tr1) cells, Cytotoxicity, Immune regulation, granzyme B"

Zhang, ping, Kate H. Gartlan, Simone A. Minnie, et al. "Type-1 regulatory T cells are critical for curative immunotherapy outcomes." Journal of Immunology 210, no. 1_Supplement (2023): 173.11. http://dx.doi.org/10.4049/jimmunol.210.supp.173.11.

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Abstract IL-10 producing CD4 +type-1 regulatory T cells (Tr1) mediate immune tolerance during chronic infection, autoimmunity, and transplantation. We previously demonstrated that eomesodermin (Eomes) promotes Tr1 cell (Eomes +IL-10 +) development after allogenic bone marrow transplantation (alloBMT). Here we define the differentiation trajectory of Tr1 cells and the functional states therein. Eomes −IL-10 −, Eomes +IL-10 −and Eomes +IL-10 +subsets (defined by mCherry and GFP expression respectively) were FACS sorted after alloBMT and transferred into secondary recipients. Eomes +IL-10 +T cell

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Liu, Jeffrey M., Pauline Chen, Brandon Cieniewicz, Alma-Martina Cepika, Rosa Bacchetta, and Maria Grazia Roncarolo. "Engineered Type-1 Regulatory T Cells as Cellular Therapy for Treatment of Immune Mediated Diseases." Journal of Immunology 204, no. 1_Supplement (2020): 87.17. http://dx.doi.org/10.4049/jimmunol.204.supp.87.17.

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Abstract Type 1 regulatory cells (Tr1) are a promising cellular product for suppression of effector T cells in immune mediated diseases, including graft-versus-host-disease (GvHD) in allogeneic hematopoietic stem cell transplantation (allo-HSCT) (Roncarolo et al. Immunity 2018). We have developed an in vitro protocol to produce Tr1 cells by lentiviral transduction of the human IL10 with a constitutive promoter into human CD4+ T cells (Locafaro et al. Molecular Therapy 2017). These engineered Tr1 cells, called LV-10, acquire a characteristic Tr1 cytokine profile (IL-10 and IFN-g high, IL-4 low

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Sultan, Hussein, and Robert Schreiber. "Abstract A075: Cytotoxic Tr1 CD4+ T cells suppress cancer immunotherapy in an antigen-specific manner." Cancer Immunology Research 13, no. 2_Supplement (2025): A075. https://doi.org/10.1158/2326-6074.io2025-a075.

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Abstract The induction of tumor-specific CD8+ cytolytic T cells (CTL) capable of destroying tumors is the ultimate outcome of cancer immunotherapy. While helper CD4+ T cells are often required to foster the induction of antitumor effector CTLs, CD4+ Foxp3+ regulatory T cells impede CTL induction and, consequently, inhibit anti-tumor immunity. Previous studies suggested that other CD4+ T cell populations might also suppress tumor immunity, but the identity, origins and function of these cells remained poorly defined. Herein, we show that FoxP3-negative type 1 regulatory T cells (Tr1) play a maj

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Gallois, Anne, Emmanuelle Godefroy, Olivier Manches, and Nina Bhardwaj. "Effect of matrix metalloproteinase-2 on CD8+ T cell and NK cell responses." Journal of Clinical Oncology 30, no. 15_suppl (2012): e21081-e21081. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e21081.

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e21081 Background: Matrix metalloproteinase 2 (MMP-2) cleaves many components of the extracellular matrix and is over-expressed in several cancers including melanoma. High levels of MMP-2 expressed by tumors are associated with later tumor stages, increased dissemination and poorer survival/prognosis. We recently identified a pathway whereby MMP-2 functions as a human endogenous “conditioner” that skews CD4+ T cells towards a detrimental/inefficient TH2 phenotype through OX40L expression and inhibition of IL-12p70 production. We unraveled the underlying mechanism: MMP-2 degrades the type I IFN

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Jahrsdoerfer, Bernd, Sue E. Blackwell, Thomas Simmet, and George J. Weiner. "Human B Cell Lines and Primary B Cells Actively Secrete Granzyme B in Response to IL-2 Family Cytokines." Blood 110, no. 11 (2007): 1340. http://dx.doi.org/10.1182/blood.v110.11.1340.1340.

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Abstract It is widely believed that the main function of B cells is antibody secretion, but not cellular cytotoxicity. Recently we found that human B cells activated with interleukin 21 (IL-21) and antibodies to the B cell receptor (BCR) or immunostimulatory oligonucleotides (CpG ODN) develop a phenotype similar to that of cytotoxic T lymphocytes. B cells treated in such a way start to secrete large amounts of granzyme B (GrB) instead of antibodies and, as in the case of B-chronic lymphocytic leukemia (B-CLL), acquire the capability to induce apoptosis in bystander B-CLL cells in a GrB-depende

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Roncarolo, Maria Grazia, Manuela Battaglia, Rosa Bacchetta, Megan Levings, and Silvia Gregori. "T-Cell-Mediated Suppression: From Bench to Bedside." Blood 122, no. 21 (2013): SCI—37—SCI—37. http://dx.doi.org/10.1182/blood.v122.21.sci-37.sci-37.

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Abstract T regulatory cells (Tregs) play a pivotal role in promoting and maintaining tolerance. Several subsets of Tregs have been identified but, to date, the best characterized are the CD4+FOXP3+ Tregs (FOXP3+Tregs), thymic-derived or induced in the periphery, and the CD4+ IL-10-producing T regulatory type 1 (Tr1) cells. In the past decade much effort has been dedicated to develop methods for the in vitro induction and expansion of FOXP3+Tregs and of Tr1 cells for Treg-based cell therapy to promote and restore tolerance in T-cell mediated diseases, and for expanding antigen (Ag)-specific Tre

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Greiner, Jochen, Yoko Ono, Susanne Hofmann, et al. "The Mutated Region of Cytoplasmatic Nucleophosmine 1 (NPM1) Elicits Both CD4+ and CD8+ T Cell Responses." Blood 118, no. 21 (2011): 2569. http://dx.doi.org/10.1182/blood.v118.21.2569.2569.

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Abstract Abstract 2569 Introduction In AML, mutations in the nucleophosmin (NPM1) gene are one of the most frequent molecular alterations and predominantly occur in AML with normal cytogenetics. Patients with NPM1 mutation without FLT3-ITD mutation show a favourable prognosis of their disease. The functional role of mutated NPM1 for the improved clinical outcome is under evaluation. Immune responses might be involved in the clinical outcome of the disease. In this work, we demonstrate both CD4+ and CD8+ T cell responses against the mutated region of NPM1. Methods The entire amino acid sequence

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Bae, Jooeun, Brandon Nguyen, Yu-Tzu Tai, et al. "Function and expression of checkpoint inhibitors and immune agonists on immune cells in monoclonal gammopathy of undetermined significance (MGUS), smoldering multiple myeloma (SMM) and MM and tumor-specific T lymphocytes." Journal of Clinical Oncology 35, no. 15_suppl (2017): 11577. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.11577.

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11577 Background: Characterization of expression and function of immune regulatory molecules in tumor microenvironment will provide the framework for developing novel therapeutic strategies. Methods: We evaluated the expression and functional impact of various immuno-regulatory molecules, PD-1, PDL-1, PDL-2, LAG3, TIM3, OX40 and GITR, on the CD138+ tumor cells, myeloid derived suppressor cells (MDSC), and T cell subsets from patients with MGUS, SMM and active MM (newly diagnosed, relapsed, relapsed/refractory), and the myeloma-specific cytotoxic T lymphocytes (CTL) induced with XBP1/CD138/CS1

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Chu, Yaya, Susiyan Jiang, Jian Jiang, et al. "Optimizing Ex-Vivo Expanded NK Cell- Mediated Antibody-Dependent Cellular Cytotoxicity (ADCC) Combined with NKTR-255 in Chronic Lymphocytic Leukemia (CLL), Follicular Lymphoma (FL), and Burkitt Lymphoma (BL)." Blood 136, Supplement 1 (2020): 23–24. http://dx.doi.org/10.1182/blood-2020-139822.

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Background: The CD20 molecule is universally expressed by normal B cells in all stages of development, from the pre-B cell up to the mature plasma cell as well as by most B cell malignancies including CLL, FL and BL (Chu/Cairo, BJH, 2016). Rituximab, a monoclonal chimeric anti-CD20 antibody, has been widely used as a chemoimmunotherapeutic regimen in the frontline therapy for patients with CD20+ BL and diffuse large B-cell lymphoma. The addition of rituximab to the CHOP backbone or to standard FAB/LMB therapy has greatly improved outcomes without significantly increasing toxicity in patients w

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Vogel, Alexander J., Thomas Petro, and Deborah Brown. "Elucidating the contribution of IRF3 to effector and memory cytotoxic T cell responses after influenza virus infection." Journal of Immunology 196, no. 1_Supplement (2016): 129.15. http://dx.doi.org/10.4049/jimmunol.196.supp.129.15.

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Abstract The role of interferon regulatory factor (IRF) 3 in initiating the type I interferon response in innate immune cells has been well studied in the context of viral infection. However, it is less clear what impact IRF3 has in shaping and maintaining adaptive immune responses. Previous reports have demonstrated that when restimulated, both CD4 and CD8 T cells from IRF3 knockout (KO) mice have significantly reduced expression of Granzyme B 30 days after infection or following secondary influenza A virus (IAV) challenge. To determine whether deficiencies in Granzyme B correlate with CTL fu

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Thèses sur le sujet "Type 1 regulatory T (Tr1) cells, Cytotoxicity, Immune regulation, granzyme B"

MAGNANI, CHIARA FRANCESCA. "Type 1 regulatory T cells: cytotoxic activity and molecular signature." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2010. http://hdl.handle.net/10281/20197.

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IL-10-producing CD4+ type 1 regulatory T (Tr1) cells, defined based on their ability to produce high levels of IL-10 in the absence of IL-4, are major players in the induction and maintenance of peripheral tolerance. Tr1 cells inhibit T cell responses mainly via cytokine dependent mechanisms. The cellular and molecular mechanisms underlying the suppression of APC by Tr1 cells are still not completely elucidated. Here, we defined that Tr1 cells specifically lyse myeloid APC through a granzyme B (GZB)- and perforin (PRF)- dependent mechanism that requires HLA class I recognition, CD54/Lymphocyte

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