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Role of Histone Methyltransferase in Breast Cancer
Published in Meenu Gupta, Rachna Jain, Arun Solanki, Fadi Al-Turjman, Cancer Prediction for Industrial IoT 4.0: A Machine Learning Perspective, 2021
Surekha Manhas, Zaved Ahmed Khan
TGF-β makes it critical to express CD103 and IL-17A/F in Treg and Th17 cells by downregulation, the expression of GFI1 up to that extent [81]. Furthermore, it also inhibits CD73 and CD39 ectonucleotidase expressions [82]. For the activation reduction of methylation marks, lysine demethylae LSD1 recruitment is carried out by GFI1 to the mentioned genetic loci. Upon TGF-β stimulation, gene expression of GFI1 gets reduced, which allows the cellular differentiation of Treg and Th17 cells optimally. T cells that lack GFI1 display an increase in IL-17A production and an increase in the expression of FOXP3 in response to transforming growth factor-beta (TGF-β) that shows similarities with G9a-deficient lymphocytes, specifically T cells [14]. As dysregulated IL-17A expression was observed in Th2 cells with a lack of G9a, the same was observed with GFI1, which is basically required to silence the expression of IL-17A found in lymphocytes [15,81]. Consequently, it is very interesting to specifically hypothesize about interactions between GFI1–G9a. Specifically, they are more critical in restraining the cellular-based responses of Treg cells along with Th17 cells, resulting in repression in the transcriptional mechanism that leads to epigenetic gene inactivation or gene silencing. For the type 11 innate lymphoid cell (ILC2) development and cellular functions, GFI1 usually acts as an important potent regulator [83]. GFI1 expression is correlated to the ST2-based receptor IL-33 expression (Il1rl1, ST2), along with the expression of GATA3. GFI1 loss in ILC2s results in the impairment of GATA3 expressions and IL-17A expression upregulation, too. It is reminiscent of the specified G9a role in ILC biology, where G9a is needed to repress the actions of genes specifically related to ILC during the development of ILC2 [69], although, unlike T cells, the GFI1 effect and potentially G9a seem to be reliant on methyltransferase-dependent repressive activity of the specific gene. By analyzing all the available dates, which suggest G9a–GFI1 are critical to performing functions in ILCs and T cells, future studies defining these interactions on the basis of molecular level might open new ways for novel therapeutics that might inhibit the dysregulated responses of Th2 cell-related to other diseases like allergies and asthma.
Topical application of celastrol alleviates atopic dermatitis symptoms mediated through the regulation of thymic stromal lymphopoietin and group 2 innate lymphoid cells
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Jae Kwon Lee, Jin Kyung Seok, Ilyoung Cho, Gabsik Yang, Kyu-Bong Kim, Seung Jun Kwack, Han Chang Kang, Yong-Yeon Cho, Hye Suk Lee, Joo Young Lee
Halim et al. (2014) reported that group 2 innate lymphoid cells (ILC2s) release Th2 cytokines. Although the population of ILC2s is lower compared to T cells, ILC2s are highly expressed in lesions of atopic dermatitis patients promoting Th2 responses (Bonefeld and Geisler 2016). The activation of ILC2 is regulated by integrating a plurality of signals, most of which are epithelial cytokines such as TSLP, IL-25 and IL-33 (Ricardo-Gonzalez et al. 2018). ILC2 cells are influenced by various lipid mediators, neuropeptides, cell-cell interaction, and cellular surface markers (Schuijs and Halim 2018). In an atopic dermatitis mouse model, the number of dermal ILC2 rose resulting in release of Th2 cytokines due to stimulation by TSLP and/or IL-33 (Salimi et al. 2013). TSLP initiates ILC2 immune responses to promote skin inflammation including atopic dermatitis (Kim et al. 2013).
From Infections to Anthropogenic Inflicted Pathologies: Involvement of Immune Balance
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Florence Lee, David A Lawrence
Growing population sizes and socio-economic shifts in disease patterns from the Pre-Neolithic (>12,000 years ago) to the present have been affecting trans-generational molding of immunity and health outcomes. Genes, culture, and ecology all contribute to shaping patterns of diet and disease (Hockett and Haws 2003; Krebs 2009). Phylogenetic environmental and humanoid microbiota have changed with shifts in diet (herbivory to carnivory) and with the practice of animal domestication, which increased zoonoses. Carnivory also shortened time to weaning and dynamics of population expansion (Psouni, Janke, and Garwicz 2012); environmental microbiota, including those in animal species, might include pathogens to humans. Thus, human populations altered the ecological landscape by generating new reservoirs for disease and influenced their own health outcomes (Hoberg et al. 2001). Host-switching of pathogens continues to be a danger, particularly as humans increase contact with wildlife due to actions such as enhanced urbanization, clear-cutting of forests, and even procurement and consumption of bushmeat. When societies did not migrate far, lived and ate in relatively small areas, and started farming, transmission of parasitic infections within communities likely rose from exposure to feces and use of fecal matter in agriculture (Cockburn 1971); such exposure may have increased worm infections. Most worm infections shift immune responses toward innate lymphoid type-2 cell (ILC2) and CD4+ helper type-2 T cell (Th2) responses, which produce imbalanced immunity by lowering ILC1 and CD4+ helper type-1 (Th1) responses. ILC2 and Th2 cells generate interleukin (IL)-4, which promotes IgE antibodies (Abs) and IL-5 and IL-13, which promotes eosinophilia, and IL-10, which with IL-4 and IL-5 suppress IL-12 mediated ILC1 and Th1 interferon-gamma (IFNγ) responses (Figure 2). Th1-mediated cell-mediated immunity (CMI) promotes host defenses against viruses and intracellular bacteria, such as Listeria and Mycobacteria. There is no apparent evidence of any ILC or CD4+ T cell subtype dominance throughout paleolithic times; however, currently, it is known that the balance between the subsets of ILC and adaptive Th populations (Figure 2) varies based upon local pathogens, human practices, chemical exposures, and genetics. Within the Anthropocene period, there has been greater distribution of chemicals and production of many new synthetics that did not exist earlier, which increased occurrences of immunomodulatory exposures and potential differential subset skewing (Table 1). Many of these relatively new chemicals utilized for varying activities altered differentially immune balance and functions leading to immunopathologies.