scholarly journals How Numbers, Nature, and Immune Status of Foxp3+ Regulatory T-Cells Shape the Early Immunological Events in Tumor Development

2013 ◽  
Vol 4 ◽  
Author(s):  
Guillaume Darrasse-Jèze ◽  
Katrina Podsypanina
Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1888 ◽  
Author(s):  
Jonadab E. Olguín ◽  
Itzel Medina-Andrade ◽  
Tonathiu Rodríguez ◽  
Miriam Rodríguez-Sosa ◽  
Luis I. Terrazas

In recent years, there has been a significant increase in the study of own and foreign human factors favoring the development of different types of cancer, including genetic and environmental ones. However, the fact that the immune response plays a fundamental role in the development of immunity and susceptibility to colorectal cancer (CRC) is much stronger. Among the many cell populations of the immune system that participate in restricting or favoring CRC development, regulatory T cells (Treg) play a major role in orchestrating immunomodulation during CRC. In this review, we established concrete evidence supporting the fact that Treg cells have an important role in the promotion of tumor development during CRC, mediating an increasing suppressive capacity which controls the effector immune response, and generating protection for tumors. Furthermore, Treg cells go through a process called “phenotypic plasticity”, where they co-express transcription factors that promote an inflammatory profile. We reunited evidence that describes the interaction between the different effector populations of the immune response and its modulation by Treg cells adapted to the tumor microenvironment, including the mechanisms used by Treg cells to suppress the protective immune response, as well as the different subpopulations of Treg cells participating in tumor progression, generating susceptibility during CRC development. Finally, we discussed whether Treg cells might or might not be a therapeutic target for an effective reduction in the morbidity and mortality caused by CRC.


2021 ◽  
Vol 23 (4) ◽  
pp. 743-748
Author(s):  
I. P. Ivanova ◽  
D. V. Dyomina ◽  
M. N. Davydova ◽  
G. V. Seledtsova

The aim of this work was to study some parameters of cellular immunity in patients with multiple sclerosis (MS). The study included 10 patients with relapsing-remitting MS aged 32 to 50 years. Diagnosis was clinically established and confirmed by magnetic resonance imaging. Patients did not receive immunosuppressive therapy for at least 6 months prior to study entry. The neurological status of all examined patients was assessed using the Kurtzke functional scale using the Extended Disability Scale (EDSS) and averaged 4.0±0.67 points, the mean number of exacerbations per year was 1.25±0.25. While studying such parameters of the immune status such as the number of T, B, NK-cells, the content of immunoglobulins, the phagocytic activity of monocytes and granulocytes, their production of reactive oxygen species, no significant differences were observed in patients with MS in comparison with the normal donor level. At the same time, we have noted an increase in the proliferative response of mononuclear blood cells to myelin antigen by 2.35 times. The content of CD4+CD45RO+CD62L+ and CD8+CD45RO+CD62L+ central memory T-cells, as well as CD8+CD45RO+CD62L- effector memory T-cells in the blood of MS patients significantly exceeded the control values (p < 0.05). Also, in MS patients, compared with healthy individuals, there was an increased level of naive IFNγ-positive CD4+CD45RO- and CD8+CD45ROT-cells (p < 0.01), and an increase in CD4+CD45RO+ and CD8+CD45RO+ memory T-cells producing IFNγg or IFNγg together with IL-4 in response to the activation (p < 0.01). Consistent with these data, there were significantly increased serum IFNγ and IL-17 levels and no changes in IL-4 levels. The relative level of naive CD4+CD25+FoxP3+, as well as induced CD4+CD25- FoxP3+ regulatory T-cells in MS patients did not significantly change compared to donor values. The results of assessing some parameters of the immune status in MS patients indicate a functional reshaping of the immune system towards the Th1 type of immune response. It is obvious that immunotropic treatment of MS should be aimed at inactivating auto-immune Tand B-lymphocytes, suppressing the production of proinflammatory mediators, and enhancing the activity of natural and induced regulatory T-cells. 


AIDS ◽  
2005 ◽  
Vol 19 (9) ◽  
pp. 879-886 ◽  
Author(s):  
Sachi Tsunemi ◽  
Tsuyoshi Iwasaki ◽  
Takehito Imado ◽  
Satoshi Higasa ◽  
Eizo Kakishita ◽  
...  

2004 ◽  
Vol 27 (6) ◽  
pp. S45
Author(s):  
Yushe Dang ◽  
Mary L (Nora) Disis ◽  
Ekram Gad ◽  
Keith Knutson

2005 ◽  
Vol 102 (26) ◽  
pp. 9253-9257 ◽  
Author(s):  
H. Nishikawa ◽  
T. Kato ◽  
I. Tawara ◽  
T. Takemitsu ◽  
K. Saito ◽  
...  

2019 ◽  
Author(s):  
Amy Li ◽  
Rebecca H. Herbst ◽  
David Canner ◽  
Jason M. Schenkel ◽  
Olivia C. Smith ◽  
...  

ABSTRACTRegulatory T cells (Tregs) can impair anti-tumor immune responses and are associated with poor prognosis in multiple cancer types. Tregs in human tumors span diverse transcriptional states distinct from those of peripheral Tregs, but their contribution to tumor development remains unknown. Here, we used single cell RNA-Seq to longitudinally profile conventional CD4+ T cells (Tconv) and Tregs in a genetic mouse model of lung adenocarcinoma. Tissue-infiltrating and peripheral CD4+ T cells differed, highlighting divergent pathways of activation during tumorigenesis. Longitudinal shifts in Treg heterogeneity suggested increased terminal differentiation and stabilization of an effector phenotype over time. In particular, effector Tregs had enhanced expression of the interleukin 33 receptor ST2. Treg-specific deletion of ST2 reduced effector Tregs, increased infiltration of CD8+ T cells into tumors, and decreased tumor burden. Our study shows that ST2 plays a critical role in Treg-mediated immunosuppression in cancer, highlighting new potential paths for therapeutic intervention.


2007 ◽  
Vol 2007 ◽  
pp. 1-10 ◽  
Author(s):  
Nathalie Cools ◽  
Peter Ponsaerts ◽  
Viggo F. I. Van Tendeloo ◽  
Zwi N. Berneman

The main function of our immune system is to protect us from invading pathogens and microorganisms by destroying infected cells, while minimizing collateral damage to tissues. In order to maintain this balance between immunity and tolerance, current understanding of the immune system attributes a major role to regulatory T cells (Tregs) in controlling both immunity and tolerance. Various subsets of Tregs have been identified based on their expression of cell surface markers, production of cytokines, and mechanisms of action. In brief, naturally occurring thymic-derivedCD4+CD25+Tregs are characterized by constitutive expression of the transcription factor FOXP3, while antigen-induced or adaptive Tregs are mainly identified by expression of immunosuppressive cytokines (interleukin-10 (IL-10) and/or transforming growth factor-β(TGF-β)). While Tregs in normal conditions regulate ongoing immune responses and prevent autoimmunity, imbalanced function or number of these Tregs, either enhanced or decreased, might lead, respectively, to decreased immunity (e.g., with tumor development or infections) or autoimmunity (e.g., multiple sclerosis). This review will discuss recent research towards a better understanding of the biology of Tregs, their interaction with other immune effector cells, such as dendritic cells, and possible interventions in human disease.


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