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Dopamine in the Immune and Hematopoietic Systems
Published in Nira Ben-Jonathan, Dopamine, 2020
The DAR subtypes differentially affect the activity of lymphocytes under various conditions. For instance, D1R-like inhibits the cytotoxic functions of CD8+ T cells, impairs the differentiation of Tregs [3], and affects the polarization of naïve CD4+ T cells toward Th17 cells [12]. D2R enhances the production of interleukin-10 (IL-10), which negatively regulates Teffs [13]. D3R facilitated the differentiation of naïve CD8+ T cells into a cytotoxic phenotype [13], and contributes to the development of naïve CD4+ T cells toward the Th1 (T helper) phenotype [14]. D3R is also involved in the migration and adhesion of T cells by inducing β1 integrin-dependent adhesion to fibronectin, potentially modulating their homing mechanism [15]. D4R affects T-cell quiescence by upregulating Krüppel-like factor-2 expression [16].
Monocyte and lymphocyte membrane markers: Ontogeny and clinical significance
Published in Gabriel Virella, Medical Immunology, 2019
Scott Sugden, Damien Montamat-Sicotte, Karen K. Yam, Joseph Murphy, Bader Yassine Diab, Virginia Litwin
One of the key players of monopoiesis is the transcription factor PU.1. High expression of PU.1 will lead to the activation of different myeloid specific factors such as interferon regulatory factor-8 (IRF8), kruppel-like factor 4 (KLF-4), and Erg1. PU.1 expression is also indispensable to the expression of macrophage colony stimulating factor receptor (M-CSFR, CD115). Macrophage colony stimulating factor (M-CSF) and IL-34 are two ligands for CD155 crucial to monocyte development.
Tissue engineering and regeneration
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
The discovery in 2006 by Shinya Yamanaka, building on the earlier work of John Gurdon, that certain types of specialised adult cells could be reprogrammed using genetic manipulation to become embryonic-like iPSCs was a major breakthrough. Using retroviral or lentiviral transfection to introduce a combination of transcription factors (OCT3/4, SOX2, and either Kruppel-like factor and C-MYC (together designated the OSKM reprogramming factors) or NANOG and LIN28), it was shown that specialised somatic cells can be reprogrammed to become stem cells. Moreover, iPSCs proliferate in vitro as efficiently as ESCs and are pluripotent, thereby circumventing concerns about the use of human embryos. Importantly, the development of iPSCs also means that, at least in principle, an intended recipient of stem cell therapy can themselves provide a source of stem cells (e.g. from a skin biopsy or blood sample) that can then be directed to differentiate into the desired specialised cell type for therapy; because such cells would be autologous they would not provoke an immunological rejection response (Figure4.3). Alternatively, iPSCs could be obtained from a number of volunteer donors selected on the basis of their HLA type and stored to create a national or international tissue bank of iPSCs. Lines of iPSCs could then be chosen from the bank to provide a fully or partially matched cell transplant for recipients, eliminating or reducing the need for immunosuppression to prevent immunological rejection.
Ferroptosis inhibition shields house ear institute-organ of corti 1 cells from free fatty acids-induced inflammatory injuries
Published in Acta Oto-Laryngologica, 2023
Xuemin Chen, Yiding Yu, Ning Yu, Weiwei Guo, Qingqing Jiang, Shiming Yang
A previous study found out that high concentrations of FFA could activate toll-like receptor 4 (TLR4)/NF-κB/interleukin 6 (IL-6) inflammatory signaling pathway by promoting the expression of Krüppel-like factor 7 (KLF7) in 3T3-L1 cells [9]. Same results illustrating the participation of FFAs in inflammatory response were also observed in human umbilical vein endothelial cells (HUVECs) [10] and HEK293 cells [11]. Several studies also revealed the relation between ferroptosis and inflammation, where ferroptosis could induce TLR4 inflammatory responses through lipid damage-associated molecular patterns (DAMPs) [12]. However, there is currently a significant paucity of knowledge regarding the underlying roles ferroptosis plays on the excessive FFA-induced ototoxicity. To help to fill this gap in knowledge, we first determined whether ferroptosis is involved in FFA-induced ototoxicity and aimed to investigate ferroptosis-dependent inflammatory response in auditory cells. Therein, the palmitate acid (PA) was utilized as a substitute for FFA.
Lef1 is transcriptionally activated by Klf4 and suppresses hyperoxia-induced alveolar epithelial cell injury
Published in Experimental Lung Research, 2022
Min Yang, Xueshan Huang, Fang Shen, Juanjuan Yi, Yanni Meng, Yanping Chen
Krüppel-like factor 4 (KLF4) is a zinc finger protein17 and could participate in many processes of cells, such as proliferation, cell cycle, apoptosis, migration and differentiation.18–21 Also, KLF4 is involved in a variety of illnesses, such as atherosclerosis,22 acute myeloid leukemia,23 and neonatal pneumonia.24 Via affecting cell apoptosis and damage of inflammation, KLF4 is associated with pneumonia.25 Alejandre Alcazar et al.21 found that Klf4 expression was diminished in lung tissue after treating the neonatal mouse with mechanical ventilation with O2-rich gas. However, the role of KLF4 in BPD remain unclear. In this study, as per bioinformatics predictions, Klf4 might well be paired with Lef1 in the promoter.
Scavenger receptor A in immunity and autoimmune diseases: Compelling evidence for targeted therapy
Published in Expert Opinion on Therapeutic Targets, 2022
Yang Xie, Yuan Jia, Zhanguo Li, Fanlei Hu
Up to now, as the first receptor identified for modified lipoproteins, the role of SR-A in atherosclerosis has been extensively studied. Therefore, agents influencing SR-A expression have been developed to treat atherosclerosis. Previous studies have shown that nobiletin, a citrus flavonoid isolated from tangerines and zerumbone, could specifically inhibit macrophage metabolism of acLDL though attenuating the expression of SR-A [136,137]. Recently, formononetin, an isoflavone extracted from Astragalus membranaceus, was determined the involvement to inhibit atherosclerosis and elucidated the underlying molecular mechanisms [138]. It was demonstrated that formononetin could increase the expression of Krüppel-like Factor 4 (KLF4), which acts as a transcription factor for negatively regulating SR-A expression at the transcriptional and translational level, and then down-regulate formation and accumulation of foam cells, which reveals a novel therapeutic approach for atherosclerosis [138].