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Immune Reconstitution after Hematopoietic Stem Cell Transplantation
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Andreas Thiel, Tobias Alexander, Christian A. Schmidt, Falk Hiepe, Renate Arnold, Andreas Radbruch, Larissa Verda, Richard K. Burt
The necessity of a thymus for development of T cells from hematopoietic stem cells (HSC) has been questioned by the finding that CD3+ T cells may be generated ex vivo from CD34+ HSC in the absence of a thymus or thymic derived factors.39 Culturing highly purified CD34+ human HSC with flt-3 ligand, stem cell factor (SCF) and interleukin-2 (IL-2) may cause differentiation into CD3+CD4+ T cells that proliferate to mitogens and have a polyclonal TCR repertoire.40 It has also been demonstrated in mice that under non-physiologic cytokine stimulation, lymph nodes may generate functional TCRαβ T cells. Oncostatin M is an interleukin-6 like cytokine normally produced by hematopoietic cells. When transgenic mice express oncostatin M under a lymphocyte specific kinase (lck) promoter (p56lck), extrathymic T cell development occurs in mesenteric lymph nodes.41-44 Administration of oncostatin M protein in non-transgenic mice also produces a similar result.42-43 Whether any human T cells may be generated in vivo but outside of a thymus under normal or cytokine (oncostatin M or IL-7)45 stimulated conditions and what phenotype, number and functional characteristics these cells will have remains controversial. However, currently, a fully functional and polyclonal TCR repertoire requires a thymus and thymic function declines with age.
Genetic variants affecting chemical mediated skin immunotoxicity
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Isisdoris Rodrigues de Souza, Patrícia Savio de Araujo-Souza, Daniela Morais Leme
Th2 cells are the primary IL-31 source in the skin (Saleem et al. 2017). However, this cytokine is also expressed by keratinocytes, fibroblasts, DCs, monocytes/macrophages, mast cells, cutaneous lymphocyte antigen (CLA)+ CD45RO+ memory T cells (Akdis et al. 2016; Bilsborough et al. 2006), and activated eosinophils (Saleem et al. 2017). IL-31 may be released after skin exposure to pathogens or following physical damage to skin tissues by UVB rays, H2O2, or staphylococcus enterotoxin B (Cheung et al. 2010; Cornelissen et al. 2011; Kunsleben et al. 2015; Sonkoly et al. 2006). After skin tissue damage occurs, keratinocytes release IL-33 that, in synergy with IL-4, upregulates IL-31 expression through the NF-ĸB pathway (Maier et al. 2014). Although, in AD, nonlesional skin also express elevated IL-31 mRNA levels (Sonkoly et al. 2006). IL-31 binds to heterodimeric IL-31 receptor A (IL-31RA) and the oncostatin M receptor (OSMR) – a receptor that enhances IL-31 binding affinity to IL-31RA (Akdis et al. 2016; Hermanns 2015). These receptors are found in T cells, keratinocytes, DCs, eosinophils, basophils, macrophages, activated monocytes, and dorsal root ganglia cells (DRG), sensory neurons responsible for the induction of itching (Akdis et al. 2016; Gibbs, Patsinakidis, and Raap 2019).
Optimizing the biodegradability and osteogenesis of biogenic collagen membrane via fluoride-modified polymer-induced liquid precursor process
Published in Science and Technology of Advanced Materials, 2023
Xiyan Li, Chuangji Li, Mengxi Su, Xinyi Zhong, Yihan Xing, Zhengjie Shan, Shoucheng Chen, Xingchen Liu, Xiayi Wu, Quan Liu, Ye Li, Shiyu Wu, Zhuofan Chen
Cells were stimulated with the conditioned medium of collagen membranes for 24 h. Total RNA was extracted using TRIzol reagent (Life Technologies, U.S.A.) following the manufacturer’s instructions. RNA was reverse-transcribed into single-stranded cDNA using the TaKaRa PrimeScriptTM Master Mix (Perfect Real Time Kit; Takara, Japan). RT-PCR was performed on an equivalent quantity of cDNA using Hieff® qPCR SYBR Green Master Mix (No Rox; Yeasen, Shanghai, China) according to the manufacturer’s instructions. The relative mRNA expression of inflammation-related genes [interleukin 1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), interleukin- 6 (IL-6), nuclear factor kappa-B1 (NFκB1), and interleukin 1 receptor antagonist (IL-1rn)], osteoclastogenesis-related genes [macrophage colony-stimulating factor (MCSF)], angiogenic factors [vascular endothelial growth factor (VEGF)], osteogenesis- and fibrosis-related genes [transforming growth factor-β1 (TGF-β1) and TGF-β3)], and collagenase [matrix metalloprotein 9, (MMP9)] were detected in the F-mBCM and blank groups. The relative mRNA expression of inflammation-related genes (IL-1β, TNF-α, IL-6, NFκB1, and IL-1rn), osteoclastogenesis-related genes (MCSF), osteogenesis- and fibrosis-related genes [TGF-β1, TGF-β3, and oncostatin M, (OSM)], and collagenase (MMP9) were detected in the SF25 and blank groups. The 2−ΔΔCt method was used to calculate relative gene expression after normalization against the housekeeping gene glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Primers used in this study are listed in Supplementary Table S1.