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Artículos de revistas sobre el tema "Tissue Treg"

Autor: Grafiati

Publicado: 25 de mayo de 2024

Última modificación: 31 de julio de 2025

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1

Li, Chaoran, Andrés R. Muñoz-Rojas, Gang Wang, Alexander O. Mann, Christophe Benoist та Diane Mathis. "PPARγ marks splenic precursors of multiple nonlymphoid-tissue Treg compartments". Proceedings of the National Academy of Sciences 118, № 13 (2021): e2025197118. http://dx.doi.org/10.1073/pnas.2025197118.

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Foxp3+CD4+ regulatory T cells (Tregs) regulate most types of immune response as well as several processes important for tissue homeostasis, for example, metabolism and repair. Dedicated Treg compartments—with distinct transcriptomes, T cell receptor repertoires, and growth/survival factor dependencies—have been identified in several nonlymphoid tissues. These Tregs are specifically adapted to function and operate in their home tissue—When, where, and how do they take on their specialized characteristics? We recently reported that a splenic Treg population expressing low levels of the transcrip

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Mailloux, Adam William, Deanne M. R. Lathers, and M. Rita I. Young. "Lewis Lung Carcinoma-derived CCL22 recruitment of T regulatory cells (B148)." Journal of Immunology 178, no. 1_Supplement (2007): LB31. http://dx.doi.org/10.4049/jimmunol.178.supp.b148.

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Abstract Two aspects of cancer progression that contribute to malignancy are the ability of the tumor to metastasize to remote locations in the body, and the ability to evade effective host anti-tumor immune responses. It has been shown that T regulatory cells (Treg) can inhibit immune effector cell function and aid in anti-tumor immune evasion. Several types of tumors have elevated Treg numbers, and it is believed that tumors may actively recruit these cell types. Treg migration is induced by several chemokines and their receptors such as CCL22 and CCR4. Here, we use flow cytometry to analyze

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Fu, Wenxian. "A tissue-resident macrophage specific coinhibitory molecule promotes regulatory T cell differentiation and stability." Journal of Immunology 196, no. 1_Supplement (2016): 125.5. http://dx.doi.org/10.4049/jimmunol.196.supp.125.5.

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Abstract CD4+ Foxp3+ regulatory T (Treg) cells are key players in immune tolerance and tissue homeostasis. Their impact on tissue homeostasis has been further reinforced by recent studies showing that Tregs in tissue control non-immunological processes. However, how Treg cell differentiation and function are influenced by tissue-derived signals remain poorly understood. We here show that a specific subset of tissue-resident macrophages can promote the differentiation and stability of Tregs. This subset of tissue-resident macrophages distinctively express complement receptor of the immunoglobul

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Camirand, Geoffrey, and David Rothstein. "Treg suppressor function in inflamed peripheral tissue and lymphoid tissue occurs through distinct mechanisms (IRC11P.426)." Journal of Immunology 194, no. 1_Supplement (2015): 197.8. http://dx.doi.org/10.4049/jimmunol.194.supp.197.8.

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Abstract The mechanisms by which Treg (CD4+Foxp3+) affect DC function and modulate immunity in inflamed non-lymphoid tissues remain poorly understood. Here, we used 2-photon intravital microscopy to visualize how Treg suppressor function operates within allografts. To restrain the immune reaction to the transplant site, we adoptively transferred effector T cells (Teff), wt Treg, or both (2-3x106 each) to B6 mice lacking 2° lymphoid organs (SLO; splenectomized LTβR-/-) 3-4 days after transplantation of BALB/c islets. Teff alone induced acute allograft rejection. However, the co-transfer of Teff

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5

Zhang, Chaoqi, Lifeng Li, Kexin Feng, Daoyang Fan, Wenhua Xue, and Jingli Lu. "‘Repair’ Treg Cells in Tissue Injury." Cellular Physiology and Biochemistry 43, no. 6 (2017): 2155–69. http://dx.doi.org/10.1159/000484295.

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Studies in mice and humans have elucidated an important role for Tregs in promoting tissue repair and restoring tissue integrity. Emerging evidence has revealed that Tregs promoted wound healing and repair processes at multiple tissue sites, such as the heart, liver, kidney, muscle, lung, bone and central nervous system. The localization of repair Tregs in the lung, muscle and liver exhibited unique phenotypes and functions. Epidermal growth factor receptor, amphiregulin, CD73/CD39 and keratinocyte growth factor are important repair factors that are produced or expressed by repair Tregs; these

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Oleinik, E. K., A. V. Churov, and V. M. Oleinik. "IMMUNOLOGICAL MEMORY: THE ROLE OF REGULATORY CELLS (TREGS)." Medical Immunology (Russia) 20, no. 5 (2018): 613–20. http://dx.doi.org/10.15789/1563-0625-2018-5-613-620.

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Memory T cells are necessary for development of the immune response and represent one of the most numerous population of human T lymphocytes. On the contrary, suppressive regulatory T cells (Tregs) may terminate the immune response and help to maintain tolerance to self-antigens. These important groups of cells are consisting of different subpopulations and retaining throughout life. However, today there is yet no clear understanding of how the relations between these two groups of cells are formed. In this work we consider possible ways of development and maintenance of CD4+ T cell memory and

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7

Salama, Paul, Michael Phillips, Fabienne Grieu, et al. "Tumor-Infiltrating FOXP3+ T Regulatory Cells Show Strong Prognostic Significance in Colorectal Cancer." Journal of Clinical Oncology 27, no. 2 (2009): 186–92. http://dx.doi.org/10.1200/jco.2008.18.7229.

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Purpose To determine the prognostic significance of FOXP3+ lymphocyte (Treg) density in colorectal cancer compared with conventional histopathologic features and with CD8+ and CD45RO+ lymphocyte densities. Patients and Methods Tissue microarrays and immunohistochemistry were used to assess the densities of CD8+, CD45RO+, and FOXP3+ lymphocytes in tumor tissue and normal colonic mucosa from 967 stage II and stage III colorectal cancers. These were evaluated for associations with histopathologic features and patient survival. Results FOXP3+ Treg density was higher in tumor tissue compared with n

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Desai, Sweta, Selene Meza-Perez, Mingyong Liu, and Troy Randall. "IL-33 mediated regulation of Tregs is tissue specific and dispensable in the omental visceral adipose tissue." Journal of Immunology 212, no. 1_Supplement (2024): 0782_6088. http://dx.doi.org/10.4049/jimmunol.212.supp.0782.6088.

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Abstract The omentum, a visceral adipose tissue in the peritoneal cavity, is a frequent site of metastasis for gastric, ovarian and various other cancers. Currently available therapies are ineffective in providing long-term tumor control, with a higher plausibility for relapse. The rapid growth of tumors in the omentum is supported by the expansion and accumulation of immunosuppressive Tregs. Additionally, we detect persistent and continuously expanding tumor specific CD8 T cells despite Treg accumulation in the omentum. Omental Tregs are a specialized population of visceral adipose tissue ass

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Moreau, Joshua Michael, Devi P. Boda, and Michael D. Rosenblum. "Regulatory T cells in skin coordinate responses to epidermal injury by initiating anti-microbial immunity while delaying tissue repair." Journal of Immunology 204, no. 1_Supplement (2020): 75.15. http://dx.doi.org/10.4049/jimmunol.204.supp.75.15.

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Abstract When barrier tissues are breached, two coordinate responses need to occur: 1) clearance of pathogens and 2) repair of damaged epithelium. Regulatory T cells (Tregs) play a major role in skin barrier repair; however, the mechanisms by which they modulate local tissue are unclear. To identify molecular pathways underpinning Treg interactions with their tissue environment, we performed single cell RNA sequencing on Tregs isolated from the skin. Our analysis revealed elevated TGFβ and integrin signaling. Specifically, we found high expression of the latent TGFβ activating integrin, αvβ8.

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10

Fu, Wenxian, Xiaomei Yuan, Bi-Huei Yang, and Yi Dong. "A tissue-resident macrophage specific coinhibitory molecule promotes regulatory T cell differentiation and stability." Journal of Immunology 198, no. 1_Supplement (2017): 223.14. http://dx.doi.org/10.4049/jimmunol.198.supp.223.14.

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Abstract CD4+Foxp3+ regulatory T (Treg) cells play a central role in the prevention of lethal autoimmunity and excessive inflammation. In contrast to their counterparts in lymphoid organs, Treg cells in non-lymphoid tissues acquire tissue-specific functional properties. While Treg tissue-tropisms are increasingly recognized, it remains poorly understood how tissue microenvironment influences Treg development, function and stability. Complement receptor of immunoglobulin family (CRIg) is a recently identified B7/CD28 family member. CRIg is exclusively expressed in tissue-resident macrophages. E

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Fu, Wenxian, Bi-Huei Yang, Xiaomei Yuan, and Yi Dong. "TCF/LEF family transcription factors in peripheral Treg homeostasis." Journal of Immunology 200, no. 1_Supplement (2018): 116.11. http://dx.doi.org/10.4049/jimmunol.200.supp.116.11.

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Abstract CD4+Foxp3+ regulatory T cells (Tregs) are key players in preventing lethal autoimmunity and excessive inflammation. However, the homeostatic dynamics of Tregs in peripheral lymphoid and non-lymphoid tissues remains poorly defined. We here report that two TCF/LEF family transcription factors, LEF1 and TCF1, play critical roles in this process. Our studies led to a revised “three-stage” model of Treg peripheral differentiation, delineated by the gradient expressions of LEF1 and TCF1. We found that LEF1− TCF1− subset was bona fide effector Tregs and exhibited a core gene signature shared

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Contreras, Amanda, Darin L. Wiesner, Brock Kingstad-Bakke, et al. "BACH2 in TRegs Limits the Number of Adipose Tissue Regulatory T Cells and Restrains Type 2 Immunity to Fungal Allergens." Journal of Immunology Research 2022 (August 5, 2022): 1–19. http://dx.doi.org/10.1155/2022/6789055.

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FoxP3+ regulatory T cells (Tregs) are essential for self-tolerance and moderating tissue-damaging inflammation. Tregs that develop and mature in the thymus are classified as central Tregs or effector Tregs based on whether Tregs predominately inhabit secondary lymphoid organs (central Tregs) or tissues (effector Tregs). By generating mice that are conditionally deficient for Bach2 in peripheral Tregs, we have examined the role of Bach2 in regulating Treg homeostasis and effector functions. Unlike global and T cell-specific Bach2-deficient mice, Treg-specific Bach2 ablation did not result in un

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Smith, Alan J., Joey Liu, Ahmet Yilmaz, Valerie Wright, David Bradley, and Willa A. Hsueh. "Obesity contributes to a dysfunctional regulatory T Cell phenotype within adipose tissue." Journal of Immunology 204, no. 1_Supplement (2020): 145.38. http://dx.doi.org/10.4049/jimmunol.204.supp.145.38.

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Abstract Adipose tissue (AT) regulatory T Cells (Tregs) play a key role in regulating inflammatory and metabolic responses. Obesity is associated with a decrease in AT Tregs as well as an increase in tissue inflammation and systemic insulin resistance in both humans and mice. We hypothesize that, in addition to the decrease in AT Treg number, there is a dysfunctional Treg phenotype caused by the increased inflammatory state within obese AT. We isolated Tregs from AT and peripheral blood(PB) from lean and obese individuals. Real-time PCR analysis was used to measure the expression of several kn

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Fan, Xiying, Bruno Moltedo, Alejandra Mendoza, et al. "CD49b defines functionally mature Treg cells that survey skin and vascular tissues." Journal of Experimental Medicine 215, no. 11 (2018): 2796–814. http://dx.doi.org/10.1084/jem.20181442.

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Regulatory T (Treg) cells prevent autoimmunity by limiting immune responses and inflammation in the secondary lymphoid organs and nonlymphoid tissues. While unique subsets of Treg cells have been described in some nonlymphoid tissues, their relationship to Treg cells in secondary lymphoid organs and circulation remains unclear. Furthermore, it is possible that Treg cells from similar tissue types share largely similar properties. We have identified a short-lived effector Treg cell subset that expresses the α2 integrin, CD49b, and exhibits a unique tissue distribution, being abundant in periphe

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Traxinger, Brianna, Sarah Vick, Valentin Voillet, et al. "Time- and tissue-dependent roles of regulatory T cells in the immune response to HSV-2." Journal of Immunology 206, no. 1_Supplement (2021): 24.19. http://dx.doi.org/10.4049/jimmunol.206.supp.24.19.

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Abstract Herpes simplex virus 2 (HSV-2) is a chronic sexually transmitted infection that causes recurrent genital ulcers and increases HIV susceptibility. Efforts to design a vaccine have assumed regulatory T cells (Tregs) restrain immune activation and impede viral clearance. However, we have previously shown that in a mouse model of vaginal primary HSV-2 infection, Treg removal leads to impaired T cell priming and migration. This suggests an alternative model where Treg function is location- and context-dependent. Additionally, research suggests that tissue-resident memory T cells (Trm) loca

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Nguyen, Vu H., Robert Zeiser, Daniel L. daSilva, et al. "In vivo dynamics of regulatory T-cell trafficking and survival predict effective strategies to control graft-versus-host disease following allogeneic transplantation." Blood 109, no. 6 (2006): 2649–56. http://dx.doi.org/10.1182/blood-2006-08-044529.

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Abstract CD4+CD25+ regulatory T cells (Tregs) suppress immune responses to alloantigens. The in vivo circulation and tissue localization of Tregs during an adaptive immune response remain unclear. We noninvasively tracked luciferase-expressing Tregs over time in an allogeneic bone marrow transplant model and demonstrated colocalization with effector T cells and initial expansion in secondary lymphoid organs before migration into inflamed tissues. Inflammation induced by irradiation and the allogeneic setting provided crucial stimuli for early Treg expansion and migration, leading to parallel r

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Geng, JieJie, Ruo Chen, Feng-fan Yang, et al. "CD98-induced CD147 signaling stabilizes the Foxp3 protein to maintain tissue homeostasis." Cellular & Molecular Immunology 18, no. 12 (2021): 2618–31. http://dx.doi.org/10.1038/s41423-021-00785-7.

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AbstractRegulatory T cell (Treg) stability is necessary for the proper control of immune activity and tissue homeostasis. However, it remains unclear whether Treg stability must be continually reinforced or is established during development under physiological conditions. Foxp3 has been characterized as a central mediator of the genetic program that governs Treg stability. Here, we demonstrate that to maintain Foxp3 protein expression, Tregs require cell-to-cell contact, which is mediated by the CD147-CD98 interaction. As Tregs are produced, CD147, which is expressed on their surface, is stimu

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Gardell, Jennifer, Daniel Boster, Justin Bowser, et al. "A NOVEL BISPECIFIC CD8 TREG MODULATOR TARGETING CYTOLYTIC CD8 REGULATORY T CELLS REDUCES PATHOGENIC CD4 T CELLS AND INFLAMMATION IN TRANSLATIONAL MODELS OF INTESTINAL AUTOIMMUNE AND INFLAMMATORY DISEASE." Inflammatory Bowel Diseases 29, Supplement_1 (2023): S12. http://dx.doi.org/10.1093/ibd/izac247.024.

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Abstract INTRODUCTION We have characterized a novel CD8 Treg network in autoimmune patient peripheral blood and tissues, in which a subset of cytolytic CD8 Treg eliminate pathogenic CD4 T cells, reducing inflammation and ameliorating disease in response to pathogenic CD4 T cell activation. We hypothesize that the CD8 Treg network is dysfunctional in patients with Celiac and Crohn’s disease, allowing pathogenic CD4 T cell expansion, the initiation of a cascade of inflammatory pathological consequences and the perpetuation of tissue destructive inflammation in Celiac disease and IBD. Here we dem

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Barros, Leandro, Cristina Ferreira, and Marc Veldhoen. "The fellowship of regulatory and tissue-resident memory cells." Mucosal Immunology 15, no. 1 (2021): 64–73. http://dx.doi.org/10.1038/s41385-021-00456-w.

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AbstractT cells located in non-lymphoid tissues have come to prominence in recent years. CD8+ tissue-resident memory (Trm) cells are important for tissue immune surveillance, provide an important line of defence against invading pathogens and show promise in cancer therapies. These cells differ in phenotype from other memory populations, are adapted to the tissue they home to where they found their cognate antigen and have different metabolic requirements for survival and activation. CD4+ Foxp3+ regulatory T (Treg) cells also consist of specialised populations, found in non-lymphoid tissues, w

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Smith, Alan J., Dharti Shantaram, Joey Liu, Valerie P. Wright, David Bradley, and Willa A. Hsueh. "Peroxisome proliferator-activated receptor gamma activation reverses adipose tissue regulatory T cell dysfunction." Journal of Immunology 206, no. 1_Supplement (2021): 113.12. http://dx.doi.org/10.4049/jimmunol.206.supp.113.12.

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Abstract Adipose tissue (AT) regulatory T Cells (Tregs) play an essential role in regulating inflammatory and metabolic responses. Obesity is associated with a decrease in AT Tregs and a corresponding increase in tissue inflammation and systemic insulin resistance in both humans and mice. In human samples, we have found Tregs isolated from visceral AT (VAT) display a dysfunctional phenotype characterized by decreased viability, decreased effector function, and increased expression of inhibitory co-receptors (PD-1 and OX40). VAT Tregs cultured with peripheral blood mononuclear cells (PBMCs) dis

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Dürr, Christoph, Dietmar Pfeifer, Annette Schmitt-Gräff, et al. "Tissue Damage and Lymphoma Derived Chemoattractive Signals Impact Regulatory T Cell Trafficking After Allogeneic Hematopoietic Cell Transplantation." Blood 114, no. 22 (2009): 3564. http://dx.doi.org/10.1182/blood.v114.22.3564.3564.

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Abstract Abstract 3564 Poster Board III-501 Regulatory T cells (Treg) have been shown previously to reduce graft-versus-host disease (GvHD) but allow for graft-versus-leukemia (GvL) effects. It is still unclear why the adoptive Treg transfer does not paralyze every immune response to the same extent. In that context Treg recruitment and localization may account for differential immune regulation. Therefore, we studied the impact of lymphoma and inflammation derived chemoattractive signals on Treg recruitment. Luciferase transgenic Treg accumulated in B cell lymphoma (BCL) tissue after allogene

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Smigiel, Kate, Elizabeth Richards, Kerri Thomas, and Dan Campbell. "CCR7 coordinates paracrine interleukin-2 cross-talk between central memory and regulatory T cells and controls the homeostatic balance between regulatory T cell subsets (P1065)." Journal of Immunology 190, no. 1_Supplement (2013): 121.4. http://dx.doi.org/10.4049/jimmunol.190.supp.121.4.

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Abstract The importance of IL-2 in immune suppression mediated by Foxp3+ Treg cells is well established. However, IL-2 is not required for Treg cell development, in vitro suppression, or to maintain total cell number; thus, the mechanism by which IL-2 controls Treg cell activity remains unclear. We demonstrate that CD44lo CD62Lhi lymphoid tissue-resident Treg cells require IL-2 for survival and maintenance, whereas CD44hi CD62Llo Treg cells with a peripheral tissue homing phenotype are IL-2 independent. We termed these subsets central (cTr) and effector Treg (eTr) cells, respectively, due to t

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Christofi, Panayiota, Chrysoula Pantazi, Nikoleta Psatha, Ioanna Sakellari, Evangelia Yannaki, and Anastasia Papadopoulou. "Promises and Pitfalls of Next-Generation Treg Adoptive Immunotherapy." Cancers 15, no. 24 (2023): 5877. http://dx.doi.org/10.3390/cancers15245877.

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Regulatory T cells (Tregs) are fundamental to maintaining immune homeostasis by inhibiting immune responses to self-antigens and preventing the excessive activation of the immune system. Their functions extend beyond immune surveillance and subpopulations of tissue-resident Treg cells can also facilitate tissue repair and homeostasis. The unique ability to regulate aberrant immune responses has generated the concept of harnessing Tregs as a new cellular immunotherapy approach for reshaping undesired immune reactions in autoimmune diseases and allo-responses in transplantation to ultimately re-

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Harrison, Ranee, Yair Botbol, Simone Sidoli, Ana-Maria Cuervo, and Fernando Macian. "Chaperone-mediated autophagy modulates regulatory T cell differentiation and function." Journal of Immunology 210, no. 1_Supplement (2023): 248.06. http://dx.doi.org/10.4049/jimmunol.210.supp.248.06.

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Abstract Autophagy has been shown to regulate many key functions of the immune system including important roles in effector and memory T cell maintenance and function. Our group showed that chaperone-mediated autophagy (CMA), a selective type of autophagy that declines with age, plays a key role in T cell activation. In this work, we have analyzed the role of CMA in generation and function of regulatory T cells (Tregs). We found that resting Tregs display high basal CMA activity, which further increases upon Treg activation. We generated Treg specific CMA-deficient mice (Foxp3:Cre-LAMP2A fl/fl

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Jacob, Jacinta, Alessia Volpe, Qi Peng, et al. "Radiolabelling of Polyclonally Expanded Human Regulatory T Cells (Treg) with 89Zr-oxine for Medium-Term In Vivo Cell Tracking." Molecules 28, no. 3 (2023): 1482. http://dx.doi.org/10.3390/molecules28031482.

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Regulatory T cells (Tregs) are a promising candidate cell therapy to treat autoimmune diseases and aid the longevity of transplanted solid organs. Despite increasing numbers of clinical trials using human Treg therapy, important questions pertaining to their in vivo fate, distribution, and function remain unanswered. Treg accumulation in relevant tissues was found to be crucial for Treg therapy efficacy, but existing blood-borne biomarkers are unlikely to accurately reflect the tissue state. Non-invasive Treg tracking by whole-body imaging is a promising alternative and can be achieved by dire

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Ho, Patrick, Jeffrey A. Bluestone, and Qizhi Tang. "Elucidating Inflammation-induced Cell Fate Decisions in Primary Human Tregs." Journal of Immunology 210, no. 1_Supplement (2023): 238.01. http://dx.doi.org/10.4049/jimmunol.210.supp.238.01.

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Abstract Adoptive regulatory T-cell (Treg) therapy is an emerging therapeutic paradigm for promoting immune tolerance in transplant and autoimmune disease settings. Prior investigations demonstrate that murine Tregs can undergo epigenetic reprogramming within chronically inflamed tissue environments, resulting in acquisition of proinflammatory functions and the capacity to exacerbate tissue damage. Despite the ramifications of Treg lineage decommitment for cell therapy applications, inflammation-induced human Treg cell fate decisions remain poorly understood. Here, we present a robust in vitro

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Valle, Jose, Jovanny Guillen, Sarah DiMichele, et al. "In silico and multi-dimensional functional interrogation of tissue Tregs reveals novel therapeutics for autoimmunity and inflammation." Journal of Immunology 210, no. 1_Supplement (2023): 234.15. http://dx.doi.org/10.4049/jimmunol.210.supp.234.15.

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Abstract Many inflammatory and autoimmune diseases present with specific organ manifestations. Understanding the immune process at the site of inflammation may offer important insights into novel therapeutic strategies. To this end, we established a biology platform that allows us to develop a deep understanding of human tissue Treg behavior to enable a next generation of therapeutics aimed at activating these regulatory circuits at the location where the disease manifests. We apply single-cell RNA sequencing and computational tools to our proprietary collection of healthy and diseased tissues

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Beppu, Lisa, Adolfo Frias, Eric Hyzny, Amanda Poholek, and Louise D’Cruz. "The role of Blimp-1 in adipose Treg differentiation and effector function." Journal of Immunology 202, no. 1_Supplement (2019): 128.11. http://dx.doi.org/10.4049/jimmunol.202.supp.128.11.

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Abstract Visceral adipose tissue regulatory T cells (VAT Tregs) protect against systemic inflammation and metabolic disease by limiting expansion of pro-inflammatory Th1 cells and M1 macrophages, and by preserving insulin sensitivity and glucose tolerance. Although their basic markers and roles have been studied, less is known about the transcriptional machinery regulating their differentiation and function. B lymphocyte-induced maturation protein-1 (BLIMP-1) is a transcriptional regulator known to be involved in the development, polarization, and maintenance of various immune cells including

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Elkins, C., Pulavendran Sivasami, Jennifer Bae, and Chaoran Li. "Cellular cholesterol homeostasis supports visceral adipose tissue (VAT) regulatory T cell (Treg) accumulation and promotes metabolic health." Journal of Immunology 210, no. 1_Supplement (2023): 76.16. http://dx.doi.org/10.4049/jimmunol.210.supp.76.16.

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Abstract A unique population of regulatory T cells (Tregs), characterized by a clonally expanded TCR repertoire and distinct transcriptional profile, is highly enriched in the visceral adipose tissue (VAT) at steady state but is lost during obesity, which exacerbates VAT inflammation and promotes metabolic disease. Therefore, understanding the factors that control the accumulation of VAT Tregs, which might be dysregulated during obesity, is important for developing novel therapies for obesity-associated metabolic diseases. Here we show that cellular cholesterol homeostasis is particularly impo

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Thornton, Angela M., Oksana F. Gavrilova, Vinay R. Penna, Patricia E. Korty, and Ethan M. Shevach. "A Treg-specific deletion of Helios causes autoimmune lipodystrophy and metabolic syndrome." Journal of Immunology 202, no. 1_Supplement (2019): 116.13. http://dx.doi.org/10.4049/jimmunol.202.supp.116.13.

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Abstract Regulatory T (Treg) cells suppress immune activation in a dominant manner and play a critical role in the maintenance of self-tolerance. A subpopulation (60–75%) of Foxp3+T regulatory (Treg) cells express the transcription factor Helios. To examine the function of Helios in Treg cells, we have generated Treg-specific Helios deficient mice (cKO, Heliosflxflx Foxp3cre). Although both Treg development in the cKO mice and their in vitro suppressor function are normal, the selective deletion of Helios in Tregs leads to slow, progressive systemic immune activation with a Th1 phenotype, hype

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Liu, Quan, Jeremy M. Lott, Lisa R. Mathews, et al. "IL-33-Driven Innate Tissue-Protective Function of ST2+ Treg Cells." Journal of Immunology 196, no. 1_Supplement (2016): 51.7. http://dx.doi.org/10.4049/jimmunol.196.supp.51.7.

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Abstract Non-lymphoid tissue-resident CD4+ Foxp3+ regulatory T (Treg) cells with the capacity to modulate non-immunological processes including organismal metabolism and tissue repair have been recently described. Notably, a large fraction of non-lymphoid tissue-resident Treg cells express ST2, the receptor for the tissue-derived cytokine and alarmin, IL-33. However, the relationship between IL-33 and ST2+ Treg cells in quiescent and pathogenic states is only starting to be understood. Using FACS and Foxp3 reporter mice, we demonstrate that ST2+ Treg cells from naïve animals are phenotypically

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Beppu, Lisa, Xiaoyao Qu, Giovanni Marrero, et al. "Blimp-1 in adipose resident Tregs controls adipocyte beiging and obesity." Journal of Immunology 204, no. 1_Supplement (2020): 81.9. http://dx.doi.org/10.4049/jimmunol.204.supp.81.9.

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Abstract Visceral adipose tissue regulatory T cells (VAT Tregs) protect against systemic inflammation and metabolic disease by limiting expansion of pro-inflammatory Th1 cells and M1 macrophages, and by preserving insulin sensitivity and glucose tolerance. Although their basic markers and roles have been studied, less is known about the transcriptional machinery regulating their differentiation and function. B lymphocyte-induced maturation protein-1 (Blimp-1) is a transcriptional regulator known to be involved in the development, polarization, and maintenance of various immune cells including

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Tomura, Michio, Ryoyo Ikebuchi, Shunsuke Teraguchi, Alexis Vandenbon, Shand H. W. Francis, and Tetsuya Honda. "A rare subset of skin-tropic regulatory T cells expressing Il10/Gzmb inhibits the cutaneous immune response." Journal of Immunology 198, no. 1_Supplement (2017): 206.14. http://dx.doi.org/10.4049/jimmunol.198.supp.206.14.

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Abstract We reported that Foxp3+ regulatory T cells (Tregs) migrating from the skin to the draining lymph node have a strong immunosuppressive effect on contact hypersensitivity (CHS) response. However, the Treg subsets that regulate the CHS response remain poorly defined. In this study, we used a combination of single-cell real-time PCR high-dimensional gene expression profiling data with spatiotemporal information about cellular movement from the mice expressing the photoconvertible protein KikGR to elucidate the role and characteristics of Treg subsets in CHS response. We found that althoug

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Ronin, Emilie, Charlotte Pouchy, Maryam Khosravi, et al. "Tissue-restricted control of established central nervous system autoimmunity by TNF receptor 2–expressing Treg cells." Proceedings of the National Academy of Sciences 118, no. 13 (2021): e2014043118. http://dx.doi.org/10.1073/pnas.2014043118.

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CD4+Foxp3+ regulatory T (Treg) cells are central modulators of autoimmune diseases. However, the timing and location of Treg cell–mediated suppression of tissue-specific autoimmunity remain undefined. Here, we addressed these questions by investigating the role of tumor necrosis factor (TNF) receptor 2 (TNFR2) signaling in Treg cells during experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. We found that TNFR2-expressing Treg cells were critical to suppress EAE at peak disease in the central nervous system but had no impact on T cell priming in lymphoid tissues at

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Fisher, James D., Stephen C. Balmert, Wensheng Zhang, et al. "Treg-inducing microparticles promote donor-specific tolerance in experimental vascularized composite allotransplantation." Proceedings of the National Academy of Sciences 116, no. 51 (2019): 25784–89. http://dx.doi.org/10.1073/pnas.1910701116.

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For individuals who sustain devastating composite tissue loss, vascularized composite allotransplantation (VCA; e.g., hand and face transplantation) has the potential to restore appearance and function of the damaged tissues. As with solid organ transplantation, however, rejection must be controlled by multidrug systemic immunosuppression with substantial side effects. As an alternative therapeutic approach inspired by natural mechanisms the body uses to control inflammation, we developed a system to enrich regulatory T cells (Tregs) in an allograft. Microparticles were engineered to sustainab

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Broady, Raewyn, Sarah Q. Crome, Jessie Yu, Jan P. Dutz, and Megan K. Levings. "Development of a Modified Skin Explant Assay to Study Treg Suppression of Th17 Cell Mediated GvHD in the Skin." Blood 112, no. 11 (2008): 5434. http://dx.doi.org/10.1182/blood.v112.11.5434.5434.

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Abstract Acute graft versus host disease (aGVHD) following haematopoietic stem cell transplantation (HCT) occurs when donor T cells infused with the graft recognise and react to histo-incompatible recipient antigens causing tissue damage. Historically, the inflammatory response in aGVHD was attributed to alloreactive CD4+ T helper and CD8+ cytotoxic T cells and alterations in cytokine production. Recently, a new CD4+ T cell subset, characterised by IL-17 production has been identified. TH17 cells produce high levels of proinflammatory cytokines, including IL-17A, IL-17F, and IL-22, and have be

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Beppu, Lisa, Raja Gopal Reddy Mooli, Xiaoyao Qu, et al. "Tregs facilitate obesity and insulin resistance via a Blimp-1-IL-10 axis." Journal of Immunology 206, no. 1_Supplement (2021): 98.01. http://dx.doi.org/10.4049/jimmunol.206.supp.98.01.

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Abstract Adipose-resident Tregs protect against systemic inflammation and metabolic disease by limiting expansion of pro-inflammatory cells, preserving insulin sensitivity and maintaining glucose tolerance. Although their basic markers and roles have been studied, less is known about the transcriptional machinery regulating their differentiation and function. B lymphocyte-induced maturation protein-1 (Blimp-1) is a transcriptional regulator known to be involved in development, polarization, and maintenance of various immune cells including CD4+ T cells. Using Blimp-1 reporter mice, we discover

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Köhne, Maren, and Marc Beyer. "ATAC-ing human tissue Treg cells." Immunity 54, no. 4 (2021): 605–7. http://dx.doi.org/10.1016/j.immuni.2021.03.014.

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Krebs, Christan F., and Oliver M. Steinmetz. "CD4+T Cell Fate in Glomerulonephritis: A Tale of Th1, Th17, and Novel Treg Subtypes." Mediators of Inflammation 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/5393894.

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Multiple studies have identified CD4+T cells as central players of glomerulonephritis (GN). Cells of the Th1 and Th17 responses cause renal tissue damage, while Tregs mediate protection. Recently, a high degree of plasticity among these T cell lineages was proposed. During inflammation, Th17 cells were shown to have the potential of transdifferentiation into Th1, Th2, or alternatively anti-inflammatory Tr1 cells. Currently available data from studies in GN, however, do not indicate relevant Th17 to Th1 or Th2 conversion, leaving the Th17 cell fate enigmatic. Tregs, on the other hand, were spec

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Larkin, Bridget M., Jyothsna Visweswaraiah, Bilian Li, et al. "Selective expansion of regulatory T cells by kidney-tethered IL2 mutein." Journal of Immunology 206, no. 1_Supplement (2021): 28.20. http://dx.doi.org/10.4049/jimmunol.206.supp.28.20.

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Abstract Regulatory T cells (Treg) play a critical role in maintaining graft tolerance following organ transplantation, and increased numbers of Tregs in solid-tissue grafts such as the kidney are associated with improved graft survival and function. Therapeutic approaches that increase Tregs offer a promising alternative to current standard-of-care treatment consisting of broad-acting immunosuppressants and their attendant side effects. While efforts to expand Tregs ex vivo for infusion into patients have shown promise, they present manufacturing and administration challenges. Low dose (LD) i

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Desai, Sweta, Selene Meza-Perez, Mingyong Liu, and Troy D. Randall. "Characterizing the role of IL-33/ST2 axis in regulating anti-tumor function by CD8 T cells during tumor metastasis in the omentum." Journal of Immunology 210, no. 1_Supplement (2023): 86.07. http://dx.doi.org/10.4049/jimmunol.210.supp.86.07.

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Abstract The omentum, a visceral adipose tissue, is a frequent site of metastasis for gastric and ovarian cancers. Advanced ovarian cancer almost always metastasizes to the omentum. Currently available therapies do not control tumor growth long-term and there is a frequent recurrence of tumor metastasis. In mice, tumor cells injected intraperitoneally implant in the omentum and grow progressively despite tumor-specific CD8 T cells. The lack of effective immunity is due in part, to rapid Treg recruitment in the omentum, which provides an immunosuppressive environment to support tumor growth. Th

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Lee, Stephen A., Nichole L. Corless, and Dean A. Lee. "Differential Expression of VEGF Receptors on Human T Cell Subsets." Blood 112, no. 11 (2008): 4906. http://dx.doi.org/10.1182/blood.v112.11.4906.4906.

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Abstract Vascular endothelial growth factors (VEGF) and their receptors (VEGFR) deliver important signals that controlling the angiogenesis of growing, injured, and malignant tissues. Expression of VEGF receptors has been described on a variety of normal and malignant leukocytes, and presumably plays a role in their trafficking to injured tissue. Differential expression of neuropilin-1 (NRP-1) has been described as a marker of regulatory T cells (Treg) in mice, and may be expressed on human thymocytes, but expression on human Tregs has not been confirmed. Moreover, earlier reports of Treg-spec

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Thornton, Angela M., Vinay Penna, Oksana Gavrilova, and Ethan M. Shevach. "Acquired Lipodystrophy is Mediated by a Treg Specific Deletion of Helios." Journal of Immunology 210, no. 1_Supplement (2023): 77.04. http://dx.doi.org/10.4049/jimmunol.210.supp.77.04.

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Abstract The selective deletion of the transcription factor, Helios, in Regulatory T Cells (Treg) leads to systemic immune activation characterized by a Th1 phenotype, hypergammaglobulinemia, and enhanced germinal center formation. Strikingly, we also observe acquired lipodystrophy, hepatic steatosis, and insulin resistance. Further analysis of the lipodystrophy had revealed a significant lymphocytic infiltrate in both the inguinal and perigonadal adipose tissue, indicating autoimmune mediated destruction of the white adipose tissue (WAT). We show here that the destruction of adipocytes is dep

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Lui, Jen Bon P., and Thomas R. Malek. "Endogenous IL-33 contributes to Treg expansion induced by IL-2/CD25, a novel IL-2 biologic developed for low-dose IL-2 therapy." Journal of Immunology 204, no. 1_Supplement (2020): 237.13. http://dx.doi.org/10.4049/jimmunol.204.supp.237.13.

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Abstract Low-dose IL-2 therapy is being advanced in patients with autoimmunity by its ability to increase Tregs. A drawback of IL-2, however, is its short-half life and potential off-target immuno-stimulatory effects. To circumvent these limitations, we developed a longer-lasting mouse IL-2/CD25 fusion protein with greater selectivity toward Tregs. IL-2/CD25 is more effective than an equivalent amount of IL-2 in controlling diabetes of NOD mice. Furthermore, compared to other tissues, IL-2/CD25 more readily expanded pancreatic Tregs, suggesting a co-factor that acts with IL-2/CD25. We consider

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Swatler, Julian, Marco De Luca, Ivano Rotella, Veronica Lise, Emilia Maria Cristina Mazza, and Enrico Lugli. "CD4+ Regulatory T Cells in Human Cancer: Subsets, Origin, and Molecular Regulation." Cancer Immunology Research 12, no. 4 (2024): 393–99. http://dx.doi.org/10.1158/2326-6066.cir-23-0517.

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Abstract CD4+CD25hiFOXP3+ regulatory T cells (Treg) play major roles in the maintenance of immune tolerance, prevention of inflammation, and tissue homeostasis and repair. In contrast with these beneficial roles, Tregs are abundant in virtually all tumors and have been mechanistically linked to disease progression, metastases development, and therapy resistance. Tregs are thus recognized as a major target for cancer immunotherapy. Compared with other sites in the body, tumors harbor hyperactivated Treg subsets whose molecular characteristics are only beginning to be elucidated. Here, we descri

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Tung, Kenneth S. K., Dominik Lenart, Agata Litwinowicz, Jessica Harakal, and Hui Qiao. "Ontogeny of tissue autoantigen expression influences the mechanism of tolerance by Foxp3+ regulatory T cells." Journal of Immunology 198, no. 1_Supplement (2017): 149.22. http://dx.doi.org/10.4049/jimmunol.198.supp.149.22.

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Abstract We studied the ontogeny of organ-specific antigen expression and its effects on inducing tolerogenic regulatory T cells (Treg). Autoimmune ovarian disease (AOD) occurred in B6AF1-AIRE null mice, associated with antibody responses to the oocyte antigen NALP5 (syn. MATER) but not zona pellucida 3 (ZP3). Between postnatal days 1 and 2, numerous ovarian ZP3- primary oocytes undergo apoptosis, providing antigens to maintain tolerance to NALP5. Although ZP3 tolerance is AIRE-independent, transient Treg-depleted adult B6AF1-DEREG mice developed AOD and autoantibody responses to both ZP3 and

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Szeponik, Louis, Paulina Akeus, Marianne Quiding Järbrink, and William Carl Ivar Rodin. "Regulatory T cells suppress the cytotoxic phenotype of T cells in intestinal tumors of APCMin/+ mice." Journal of Immunology 202, no. 1_Supplement (2019): 138.14. http://dx.doi.org/10.4049/jimmunol.202.supp.138.14.

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Abstract The presence of activated T cells in colorectal cancer (CRC) tissues is a strong predictor of patient survival. Our previous research have shown that regulatory T cells (Treg) are able to reduce T-cell transendothelial migration in vitro and accumulation of effector T cells in intestinal tumors in vivo in a murine model for intestinal adenomas (APCMin/+). In this study we investigated the effect of Treg depletion on the cytotoxic potential of conventional αβ T cells and γδ T cells in intestinal adenomas. We used the APCMin/+ \DEREG mouse model, which harbours a high affinity diphtheri

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Jing, Yi, Yuelin Kong, Denise Trout, Matthew L. Bettini, and Maria Bettini. "Insulin specific TCR repertoire analysis reveals functional diversity of Treg TCRs." Journal of Immunology 208, no. 1_Supplement (2022): 104.04. http://dx.doi.org/10.4049/jimmunol.208.supp.104.04.

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Abstract Regulatory T cells (Tregs) are critical in preventing autoimmunity and express a unique TCR repertoire with high affinity to self-antigens. However, whether Treg and effector T cell (Teff) TCR repertoires are similarly divergent in the context of autoimmunity, and whether Tregs are able to maintain TCR affinity advantage has not been clearly defined. Insulin tetramer positive Tregs isolated from pancreatic islets of NOD mice showed a higher level of self-reactivity (CD5) and TCR signaling (Nur77-GFP) than Teffs specific to the same epitope. We isolated and sequenced insulin tetramer+

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Kalekar, Lokesh A., Jarish N. Cohen, Nicolas Prevel, et al. "Regulatory T cells in skin are uniquely poised to suppress profibrotic immune responses." Science Immunology 4, no. 39 (2019): eaaw2910. http://dx.doi.org/10.1126/sciimmunol.aaw2910.

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At the center of fibrosing diseases is the aberrant activation of tissue fibroblasts. The cellular and molecular mechanisms of how the immune system augments fibroblast activation have been described; however, little is known about how the immune system controls fibroblast function in tissues. Here, we identify regulatory T cells (Tregs) as important regulators of fibroblast activation in skin. Bulk cell and single-cell analysis of Tregs in murine skin and lungs revealed that Tregs in skin are transcriptionally distinct and skewed toward T helper 2 (TH2) differentiation. When compared with Tre

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Ho, Patrick, Jeffrey Bluestone, and Qizhi Tang. "Elucidating inflammation-induced cell fate decisions in primary human Tregs." Journal of Immunology 212, no. 1_Supplement (2024): 0420_4423. http://dx.doi.org/10.4049/jimmunol.212.supp.0420.4423.

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Abstract Adoptive regulatory T-cell (Treg) therapy has remarkable efficacy in promoting immune tolerance in preclinical models of transplantation and autoimmune disease. However, lineage-tracing studies have revealed that Tregs can undergo epigenetic reprogramming in chronically inflamed tissue environments, resulting in the acquisition of proinflammatory functions and the capacity to exacerbate autoimmunity. Despite intense interests in developing Treg therapy for humans, inflammation-induced human Treg lineage-decommitment remains poorly understood. Here, we present a robust in vitro model o

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