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Intraepithelial T cells: Specialized T cells at epithelial surfaces
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Although genetic programming is involved in γδ gene rearrangements, selective TCRγδ-associated signals may also control the specific gut-homing ability of the TCRγδ+ precursors. For example, TCRγδ transgenic G8 thymocytes specific for the MHC class Ib molecules, T10b/T22b, differentiate in the presence of their cognate antigen, and directly home to the gut but nowhere else. Consistent with this, functional sphingolipid receptor, S1P1, is not required for egress of TCRγδ+ nIET precursor thymocytes. Thymic programming of TCRγδ progenitors is imprinted at the DN3 stage and requires a full γδ TCR together with CD3 components and functional linker for activation of T cells. Whether thymic ligand engagement is required for nIET precursors expressing an endogenous TCRγδ is still unclear, but it was shown for fetal TCRVγ5+ thymocytes that interaction with Skint1 on thymic epithelial cells induced a strong TCR signal that mediated induction of Tbx21 (or T-bet). The absence of ligand engagement resulted in the maintenance of Sox13 and induction of RORγt, mediating differentiation into distinct functional subsets.
Immunopathogenesis of Vanishing Bile Duct Syndromes
Published in Gianfranco Alpini, Domenico Alvaro, Marco Marzioni, Gene LeSage, Nicholas LaRusso, The Pathophysiology of Biliary Epithelia, 2020
John M. Vierling, Marius Braun, Haimei Wang
Antinuclear antibodies (ANAs) are detected in approximately 52% of patients with PBC and are the only disease-specific autoantibodies detected in the AMA-negative variant AIC.63 Three PBC-specific ANAs react with autoantigens within the nuclear membrane: 1) gp210, a 210 kDa transmembrane nuclear pore glycoprotein involved in nuclear membrane attachment of pore complexes; 2) nuclear pore glycoprotein p62; and 3) inner nuclear membrane protein lamin B receptor (LBR) that binds nuclear lamins and double-stranded DNA and may anchor nuclear lamins and heterochromatin during interphase. Autoantibodies to gp210 and p62 are mutually exclusive. Although disease specific, the prevalence of these ANAs varies considerably. In contrast to the absence of prognostic significance of AMAs, anti-gp210 autoantibodies were significantly associated with fatality. A minority of patients also have ANAs that react with an antigen referred to as Sp 100, which colocalize with promyelocytic leukemia protein in nuclear dots, and the SOX13 nuclear transcription factor. The relevance of these autoantibodies to immunopathogenesis is unknown.
SOX13 dependent PAX8 expression promotes the proliferation of gastric carcinoma cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Liang-Yu Bie, Dan Li, Yan Wei, Ning Li, Xiao-Bing Chen, Su-Xia Luo
SRY-BOX13 (SOX13) has been shown a key regulator for cell stemness and cell differentiation in normal and cancer tissues by regulating Wnt/β-catenin signalling [16,17]. Since SOX13 shares more than 60% homology with HMG-box, SOX13, usually shown as a transcription factor, can bind to the HMG-box motif of the target gene promoter, and recruit other transcription molecules to form a transcriptional complex [18,19]. In recent years, SOX13 has been found highly expressed in tumours, and cancer patients with a high SOX13 expression often have a poor survival prognosis, making it a potential tumour biomarker for diagnosis and treatment in malignant tumour [20]. However, the role of SOX13 on tumourigenesis in human gastric cancer has not been explored.
γδT17/γδTreg cell subsets: a new paradigm for asthma treatment
Published in Journal of Asthma, 2022
Yi-En Yao, Cai-Cheng Qin, Chao-Mian Yang, Tian-Xia Huang
Regarding the mechanism, Sox13 induces the expression of BLK, which is a crucial signal transducer for the development of γδT17 cells (37). Together with Sox4, it controls the expression of RORγt20, which is the main "Type 17" transcription factor of γδT and similar cells (39–41). Interestingly, the locus encoding RORγt is controlled by epigenetic mechanisms in γδT cells, which accumulates positive modifications of histone H3 related to gene transcription in CD27-CCR6+ subpopulations that produce γδT17 cells. Therefore, there is a complex regulatory mechanism of differentiation and transcription in γδT17 cells (30,40,42). For "pre-programmed" mouse γδT cells, their peripheral activation is usually faster and simpler than other lymphocytic cells carrying rearranged antigen receptors. In fact, even in the absence of TCR stimulation, IL-1β and IL-23 stimulation were sufficient to trigger IL-17 secretion by CD27-CCR6+ γδT cells in vitro, however stimulations with TGF-β or IL-6 alone led to no effect (17,32,41,43). The innate pattern activated by mouse γδT17 cells is highlighted by its rapid response to pathogen-related molecules such as lipopolysaccharide or lipoproteins (ligands of receptor TLR4 and TLR2, respectively). Such rapid response is mediated by IL-1β and IL-23 derived from bone marrow cells, such as macrophages (43–45). In addition, IL-1β and IL-23 could also induce the production of IFN-γ by γδT17 cells (40,41). This peripheral plasticity of γδT17 cells is shown by the permissive chromatin configuration of the IFN-γ locus in CD27-CCR6+ γδT cells (40), which occurs when considerable inflammation occurs in the body (46–48).