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Parasite Versus Host: Pathology and Disease
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
In an experiment, mice that are FoxP3— are infected with Schistosoma mansoni. FoxP3 is an important transcription factor expressed in Treg cells. Thus, a Treg response is absent in these mice. Predict the likely outcome of infection in these mice, and explain this outcome, based on the lack of a Treg response.
Biomarkers for the Immune Checkpoint Inhibitors
Published in Sherry X. Yang, Janet E. Dancey, Handbook of Therapeutic Biomarkers in Cancer, 2021
Weijie Ma, Sixi Wei, Eddie C. Tian, Tianhong Li
Naturally occurring Tregs express FOXP3 and act to suppress anti-tumor immune responses; therefore, the decrease of FOXP3/Tregs in patients with a positive clinical outcome supports the idea that an immune-active TME is necessary for a favorable response to ICIs. Similarly, in a previous analysis, patients who did not respond to ipilimumab tended to have a greater Treg response in peripheral blood than those who responded [62]. It is possible that a lower frequency of FOXP3/Tregs in the peripheral blood of clinical responders reflects migration to the tumor site. Surprisingly, retrospective studies of patients treated with ipilimumab or tremelimumab have shown that high baseline expression of FOXP3 within the tumor microenvironment is associated with a better prognosis [63]. In addition, the presence of CD4+FOXP3+CD25hi Tregs is also associated with poor prognosis due to the suppression effect in tumor response [64].
Etiopathogenesis
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Dario Didona, Biagio Didona, Giovanni Paolino, Raffaele Dante Caposiena Caro
Forkhead box P3 (FOXP3) gene localized at Xp11.23 region encodes the protein scurfin. The gene plays a pivotal role in the development and function of CD25+CD4+ regulatory T cells. In addition, FOXP3 gene mutations causes the IPEX (immunodysregulation polyendocrinopathy enteropathy X-linked) syndrome, characterized by an association of several autoimmune diseases, including diabetes mellitus type 1, thyroid autoimmune diseases, inflammatory bowel diseases, allergic diseases (e.g., atopic dermatitis, food allergies), and vitiligo [10].
Investigation of possible associations between tryptophan/kynurenine status and FOXP3 expression in colorectal cancer
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2022
Ebru Nur Ay, Şeyda Demirkol, Mehmet Tolgahan Hakan, Cem Horozoğlu, Soykan Arıkan, Mehmet Baki Doğan, Filiz Akyüz, Ceylan Özsoy Hepokur, İlhan Yaylım
FOXP3 (Forkhead box P3, Transcription factor fork box P3) is a protein with 431 amino acids belonging to the fork-helix transcription factor family, located on the X chromosome p11.23 and encoded from the FOXP3 gene. FOXP3 has been identified as a marker of CD4 + CD25 + regulatory T cells and is an essential protein of immunosuppressive functions. FOXP3 has been shown to limit antitumor immune responses during tumor progression [11]. Considering the gene expression levels of the FOXP3 gene that may be related to gene polymorphisms, the reason for the FOXP3 gene expression changes has not been fully elucidated. However, various studies have shown that FOXP3 immune staining in colorectal cancer tissues may decrease due to the different localization of FOXP3 molecule according to the cancer cell type . This issue can be explained due to the its passing of FOXP3 molecule from nucleus to cytoplasm in the tumoral tissues[12]. More studies are needed to understand whether these changes in FOXP3 gene expression levels in tumor cells have the potential of clinical significance as a prognostic factor and its relationship with the differences in FOXP gene expression in tumor cells [3,4].
The molecular structure and biological functions of RNA methylation, with special emphasis on the roles of RNA methylation in autoimmune diseases
Published in Critical Reviews in Clinical Laboratory Sciences, 2022
Wanwan Zhou, Xiao Wang, Jun Chang, Chenglong Cheng, Chenggui Miao
An imbalance in the regulatory T (Treg) cells and effector lymphocytes can contribute to the pathogenesis of autoimmune diseases. Treg cells promote immune tolerance and maintain immune system homeostasis. In autoimmune diseases, including RA, SLE, type 1 diabetes, and multiple sclerosis, the number or function of the Treg cells isolated from peripheral blood decline. Therapeutic regulation of Treg cells may be an effective way to treat autoimmune diseases [13,14]. Treg cells expressing Forkhead box protein P3 (Foxp3) are critical for self-tolerance. Foxp3, a key transcription factor in Treg cells, is crucial in maintaining their immunosuppressive function. Foxp3 can be heterogeneous or unstably expressed in Treg subpopulations and can affect the pathological mechanisms of autoimmune diseases. Regulating Treg cell differentiation during DNA transcription or protein modification may improve the success rate of Treg cell-modified immunotherapy [15,16].
Evaluation of CD4+CD25+FOXP3+ regulatory T cells and FOXP3 mRNA in premature ovarian insufficiency
Published in Climacteric, 2020
J. Xiong, R. Tan, W. Wang, H. Wang, D. Pu, J. Wu
The FOXP3 gene is primarily expressed in CD4+CD25+ Treg cells in normal physiological conditions; FOXP3 regulates the activation of Treg cells and is an analytical biomarker of autoimmune activity. The double role of FOXP3 as a transcriptional repressor and activator has been demonstrated10. The literature indicates that polymorphisms in the FOXP3 gene may change FOXP3 functionally or quantitatively, therefore leading to the lack of functional CD4+CD25+ Treg cells, resulting in various autoimmune diseases9, including recurrent idiopathic abortion26 and endometriosis27. The results of the present study showed for the first time that the mRNA levels of the FOXP3 transcriptional factor are significantly decreased in the peripheral blood of POI patients, which may result in the insufficiency of the CD4+CD25+ Treg cell immune suppressive function.