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Patient assessment
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
The chronicity of psoriasis is explained by a process known as a positive chemotactic feedback loop; where pro-inflammatory chemokines such as the aforementioned IL-17 and TNF stimulates keratinocytes to synthesise a further chemotactic agent known as chemokine C-C motif ligand 20 (CCL20). CCL20 attracts T-lymphocytes to a psoriatic plaque, and on arrival, they are stimulated themselves to secrete more pro-inflammatory chemokines. The overall effect of this is one of perpetual inflammation, with a constant supply of T-lymphocytes which are autoactivated to secrete inflammatory chemokines and maintain a permanent inflammatory state.
M cells and the follicle-associated epithelium
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Hiroshi Ohno, Marian Neutra, Ifor R. Williams
FAE cells differ from villus cells in their ability to release certain chemokines that attract immune cells toward the FAE and thus to sites of organized lymphoid tissue. In the small intestine of mice and humans, for example, chemokine CCL20, also designated macrophage inflammatory protein-3α (MIP-3α), is constitutively expressed in the FAE but not in the villus epithelium (Figure 15.2). CCL20 attracts subpopulations of DCs and lymphocytes that express the chemokine receptor CCR6. Mice that lack CCR6 have lower numbers of CD11c+ DCs in the subepithelial dome regions of Peyer's patches and have an impaired humoral immune response to orally administered antigen and certain enteropathogenic viruses. Cells of the mouse FAE also express CCL9 (analogous to CCL23 in humans), which attracts CCR1-expressing myeloid DCs, and CXCL16, which attracts CXCR6-expressing B and T lymphocytes into Peyer's patches.
Cell Recruitment for Intervertebral Disc
Published in Raquel M. Gonçalves, Mário Adolfo Barbosa, Gene and Cell Delivery for Intervertebral Disc Degeneration, 2018
Catarina Leite Pereira, Sibylle Grad, Mário Adolfo Barbosa, Raquel M. Gonçalves
CCL20 expression in NP cells has also been reported. Both CCL20 and its receptor CCR6 have been associated with IVD degenerative conditions (Zhang et al. 2013b). CCR6, the only receptor of CCL20, is specifically expressed on the Th17 cell surface and is related to the recruitment of these cells in several inflammatory diseases; higher levels of IL-17 (T-helper 17 and Th17 associated cytokine) have been observed in patients with IVD degeneration (Shamji et al. 2010). This interaction was reinforced in a study using a rat model; Zhang et al. (2016) could show a positive correlation between the expression levels of CCL20-, CCR6-, and IL-17-producing cells, suggesting that the recruitment of these cells to degenerated IVD tissues occurred via the CCL20/CCR6 system in vivo. An association between AF cell migration and CXCL10 had already been established, suggesting a role of this chemokine in AF homeostasis and repair (Hegewald et al. 2012). Taken together, these results demonstrate the involvement of several chemotactic molecules in the disc degeneration pathogenesis. Moreover, most of the studies could identify cytokines and chemokines that are directly or indirectly related to the recruitment of immune cells, thereby intensifying the inflammatory response and the release of neurotrophines, promoting pain. The study of these molecules is relevant not only for the design of new therapies, by targeting symptomatic discs and the associated inflammation, but also for understanding the players in stem cell recruitment for repair.
Reconciling two opposing effects of radiation therapy: stimulation of cancer cell invasion and activation of anti-cancer immunity
Published in International Journal of Radiation Biology, 2023
Treg cells are a subset of T cells which negatively regulate Teff cell function and proliferation by up-regulating intracellular cyclic AMP (Bopp et al. 2007). Short-range suppressive factors, such as TGFβ, IL-10, and IL-35 have been shown to be secreted by Treg cells and to suppress Teff cell function (Nakamura et al. 2001; Collison et al. 2007). In addition, Treg cells can act as a cytokine ‘sink’ by depriving T cells of IL-2, which is required for their proliferation and differentiation (Pandiyan et al. 2007). Treg cells were shown to limit response to RT in patients with HNSCC and in an orthotopic mouse model of oral cavity SCC (Oweida, Hararah, et al. 2018; Oweida, Sabri, et al. 2018; Oweida et al. 2019). Although several Treg chemokines exist, CCL20 is the most prominent in cancer. In HNSCC, Tregs expressing the CCL20 receptor, CCR6, were shown to have superior suppressive activity than Tregs without CCR6 expression (Yamazaki et al. 2008). In colorectal cancer, tumor cell-derived CCL20 was shown to recruit Tregs and promote chemoresistance through NFκB (Wang et al. 2019). CCL20 has also been shown to be a negative predictive marker for survival of patients with esophageal SCC (Liu et al. 2015). In a murine model of HNSCC, CCL20 was shown to be induced by RT and promoted Treg cell infiltration into tumors, resulting in a dampened response to RT (Oweida, Hararah, et al. 2018; Oweida, Sabri, et al. 2018; Oweida et al. 2019).
Mechanical strain mimicking breathing amplifies alterations in gene expression induced by SiO2 NPs in lung epithelial cells
Published in Nanotoxicology, 2019
Carmen Schmitz, Jennifer Welck, Isabella Tavernaro, Marianna Grinberg, Jörg Rahnenführer, Alexandra K. Kiemer, Christoph van Thriel, Jan G. Hengstler, Annette Kraegeloh
In this study, for the first time, the effects of silica NPs on gene expression of mechanically stretched lung epithelial cells were analyzed. Only under the combined conditions, upregulation of nine genes related to proinflammatory responses (Table 4) was induced. According to the gene array data, the chemokine CCL20 was among the strongest upregulated genes. CCL20 is known to recruit immature dendritic cells and subpopulations of T-lymphocytes and B cells (Schutyser et al. 2003). CXCL8, encoding for the neutrophil attracting chemokine IL-8, was also markedly upregulated (Table 4). In comparison, no increase in the secretion of IL-8 by stretched and silica NPs treated primary endothelial cells (HUVEC) was found by Freese et al. (2014). In addition, in this study, a moderate (2-4-fold) upregulation was observed for CCL2, CXCL1, CXCL2, CXCL3, IL6, ICAM1, and PTX3. An augmented expression of ICAM-1 induced by silica NPs combined with mechanical strain was also found in endothelial cells (Huh et al. 2010). In the same study, 12 nm colloidal silica NPs were shown to increase ROS generation when applied to stretched alveolar epithelial cells.
Acteoside relieves mesangial cell injury by regulating Th22 cell chemotaxis and proliferation in IgA nephropathy
Published in Renal Failure, 2018
Lu Gan, Xiaozhao Li, Mengyuan Zhu, Chen Chen, Huimin Luo, Qiaoling Zhou
CD4+ T lymphocytes from patients with IgAN were isolated and purified using a CD4+ T cell isolation kit according to the manufacturer’s instructions (Miltenyi Biotec, Bergisch Gladbach, Germany). Purified CD4+ T lymphocytes from each IgAN patient were separated into three groups, i.e., control group, HMC group and acteoside group. These CD4+ T lymphocytes were added into the upper chambers of a 24-well transwell plate (Corning Costar, New York, USA) in RPMI-1640 medium with 0.5% FBS in a final volume of 100 μL. The lower chambers of transwell plate were filled with 600 μL of supernatant of cultured human mesangial cells (HMCs) (purchased from Central South University Advanced Research Center, Hunan, China). Acteoside (40 mM; purchased from Sichuan Medo Pharmaceutical Stock Co., Ltd, Sichuan, China) was used to interfere the Th22 cell chemotaxis. The transwell chambers were placed at 37 °C in 5% CO2 for 5 h. Th22 cells migrated into the lower chamber were analyzed by flow cytometry, and assigned a chemotaxis index (chemotaxis index = number of migrated Th22 cells in each experiment group ÷ number of migrated Th22 cells in response to medium alone). The concentrations of CCL20, CCL22 and CCL27 were quantified by using enzyme-linked immunosorbent assay (ELISA) kits (R&D, MN, USA) according to the manufacturer’s instructions.