Analysis of regulatory T cells and CTLA-4 expression in pregnant women according to seropositivity to Toxoplasma gondii

Parasitology ◽  
2020 ◽  
Vol 147 (7) ◽  
pp. 810-815
Author(s):  
Karine Rezende-Oliveira ◽  
César Gómez-Hernández ◽  
Marcos Vinicius da Silva ◽  
Fernanda Rodrigues Helmo ◽  
Virmondes Rodrigues

AbstractPregnancy is considered a period in which immunomodulation occurs, although it is important for the maintenance of the foetus, could contribute to infections as Toxoplasma gondii. Immune response cells such as regulatory T cells participate in this immunomodulation, and surface molecules such as CTLA-4 develop an immunosuppressive role, could contribute to the establishment of the parasite. This study aimed to evaluate the presence of regulatory T cells and the expression of CTLA-4 in parturient and non-pregnant seropositive and seronegative for anti-T. gondii antibodies. Sixty-two participants were evaluated, 14 parturient with negative serology, 23 parturient with positive serology, 16 non-pregnant women seronegative and 9 non-pregnant women seropositive. Immunophenotyping was performed for characterize TCD4+Foxp3+ cells, T CD4+CD25-Foxp3+, TCD4+CD25highFoxp3+, TCD4+CTLA-4+, TCD4+CD25-CTLA-4+ and TCD4+CD25highCTLA-4+. We observed a lower level of CD4+CD25highFoxp3+ cells from seropositive parturient compared with seropositive non-pregnant cells. Significative levels of CD4+CD25-Foxp3+ cells from seronegative pregnant were observed compared with seropositive pregnant cells. Furthermore, the higher level of CD4+CD25-CTLA-4+ cells populations was detected in seropositive pregnant cells compared with seropositive non-pregnant. Although a significant increase in CTLA-4 cells was observed in pregnant women positive for anti-T. gondii antibodies, this increase did not cause a risk of reactivation of the infection.

2015 ◽  
Vol 17 (8) ◽  
pp. 586-595 ◽  
Author(s):  
Jonadab E. Olguín ◽  
Jacquelina Fernández ◽  
Nohemí Salinas ◽  
Imelda Juárez ◽  
Miriam Rodriguez-Sosa ◽  
...  

2016 ◽  
Vol 85 (4) ◽  
pp. 323-326
Author(s):  
Magdalena Frydrychowicz ◽  
Maciej Boruczkowski ◽  
Agata Kolecka-Bednarczyk ◽  
Renata Jenek ◽  
Joanna Rosołowska ◽  
...  

Regulatory T cells (Tregs) is heterogenic subpopulation of T cells that is able to suppress function of effector cells during the immune response. Among them are natural (nTreg) and induced Treg (Tr1, Th3, CD4+CD25-). CD25, CD45Ro, CD152, GITR, LAG-3, several adhesion molecules, chemokine receptors as well as Toll-like receptors are present on the surface of Treg. Mechanism of suppression used by nTreg is not completely understood.


2014 ◽  
Vol 6 (241) ◽  
pp. 241ra78-241ra78 ◽  
Author(s):  
S. Kasagi ◽  
P. Zhang ◽  
L. Che ◽  
B. Abbatiello ◽  
T. Maruyama ◽  
...  

2020 ◽  
Vol 21 (21) ◽  
pp. 7849
Author(s):  
Narendra Prasad Singh ◽  
Mitzi Nagarkatti ◽  
Prakash Nagarkatti

Aryl hydrocarbon receptor (AhR) was identified in the early 1970s as a receptor for the ubiquitous environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin), which is a member of halogenated aromatic hydrocarbons (HAHs). TCDD was found to be highly toxic to the immune system, causing thymic involution and suppression of a variety of T and B cell responses. The fact that environmental chemicals cause immunosuppression led to the emergence of a new field, immunotoxicology. While studies carried out in early 1980s demonstrated that TCDD induces suppressor T cells that attenuate the immune response to antigens, further studies on these cells were abandoned due to a lack of specific markers to identify such cells. Thus, it was not until 2001 when FoxP3 was identified as a master regulator of Regulatory T cells (Tregs) that the effect of AhR activation on immunoregulation was rekindled. The more recent research on AhR has led to the emergence of AhR as not only an environmental sensor but also as a key regulator of immune response, especially the differentiation of Tregs vs. Th17 cells, by a variety of endogenous, microbial, dietary, and environmental ligands. This review not only discusses how the role of AhR emerged from it being an environmental sensor to become a key immunoregulator, but also confers the identification of new AhR ligands, which are providing novel insights into the mechanisms of Treg vs. Th17 differentiation. Lastly, we discuss how AhR ligands can trigger epigenetic pathways, which may provide new opportunities to regulate inflammation and treat autoimmune diseases.


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.


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