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Leukotrichia in Vitiligo
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
M. Ramesha Bhat, Jyothi Jayaraman
Follicular melanocytes originate in the neural crest and migrate to the dermis and epidermis. Recruitment of neural crest cells is regulated by microphthalmia transcription factor (Mitf) and paired box transcription factor 3 (Pax3), which stimulate enzymes related to melanin synthesis. Migration of melanoblasts is controlled by endothelin B receptor type B and c-KIT oncogene receptor. Mutation of these is responsible for leukotrichia in piebaldism [7].
Principles of Clinical Diagnosis
Published in Susan Bayliss Mallory, Alanna Bree, Peggy Chern, Illustrated Manual of Pediatric Dermatology, 2005
Susan Bayliss Mallory, Alanna Bree, Peggy Chern
Major pointsWaardenburg syndrome type IDepigmented patches of the skin and hairHeterochromia iridesDeafnessDystopia canthorumBroad nasal rootSynophrys (confluence of the medial eyebrows)Hypoplasia of the nasal alaeGene/gene locus: PAX 3 gene (transcription factor for melanocyte proliferation and migration from the neural crest)/2q35Autosomal dominantWaardenburg syndrome type IISimilar to type I except without dystopia canthorumGene/gene locus: MITF gene (microphthalmia-associated transcription factor)/3p14.1-12.3 and othersAutosomal dominantWaardenburg syndrome type III (Klein–Waardenburg syndrome)Similar to type I with limb abnormalitiesGene/gene locus: PAX 3 gene/2q35Autosomal dominantWaardenburg syndrome type IVSimilar to type I with Hirschsprung diseaseGene/gene locus: endothelin B receptor gene/20q13.2-q13.3Autosomal recessive
Facing the future: challenges and opportunities in adoptive T cell therapy in cancer
Published in Expert Opinion on Biological Therapy, 2019
Isabelle Magalhaes, Claudia Carvalho-Queiroz, Ciputra Adijaya Hartana, Andreas Kaiser, Ana Lukic, Michael Mints, Ola Nilsson, Hans Grönlund, Jonas Mattsson, Sofia Berglund
The hypoxia resulting from vessel compression and high interstitial pressure in itself suppresses the cytotoxic effects of T and NK cells; recruits myeloid-derived suppressor cells (MDSCs) [118], Tregs, and TAMs [119]; and stimulates programmed death-ligand 1(PD-L1) expression [120]. An important feature of the tumor endothelial cells (TECs) in the tumor blood vessels is FasL expression, which induces apoptosis in cells intravasating through the vessel walls. Since Tregs are somewhat protected from this effect by a high expression of c-FLIP, FasL expression by TEC selectively depletes conventional T cells, especially CD8+ T cells, while promoting Tregs in the tumor microenvironment [121]. The endothelin B receptor, that is also upregulated on TECs, further limits intravasation of TILs [122].
Relationship between G proteins coupled receptors and tight junctions
Published in Tissue Barriers, 2018
Lorenza González-Mariscal, Arturo Raya-Sandino, Laura González-González, Christian Hernández-Guzmán
Endothelins are 21-amino acid peptides that constrict blood vessels and raise blood pressure. In rat, status epilepticus induced the activation of endothelin B receptor, leading to nitric oxide synthase (eNOS) mediated activation of MMP-9 and degradation of claudin-2, occludin and ZO-1 in endothelia from brain cortex.142 Moreover, transgenic mice with endothelial endothelin-1 over-expression show more severe vascular permeability and BBB breakdown after transient middle cerebral artery occlusion. The brain of these animals displayed oxidative stress, edema, increased MMP-2 expression, BBB leakage and a decreased occludin level. Interestingly, endothelin-1 antagonist A-147627 partially normalized the infarct volume and neurological deficit in these mice, highlighting the contribution of endothelin receptor activation to BBB breakdown under ischemia.143
Tumor necrosis factor alpha expression is increased in maternal microvascular endothelial cells in preeclampsia
Published in Hypertension in Pregnancy, 2021
TNFα is a 17 kDa pro-inflammatory Th1 cytokine protein that forms homotrimers of 51 kDa (4). The TNFα ligand exerts its biological function through interaction with its two transmembrane receptors TNFR1 and TNFR2. TNFR1 is expressed in most tissues and is the key mediator of TNFα signaling. The binding of TNFα to its receptors triggers several intracellular signaling pathways including the activation of NFκB, MAPK, JNK and p38 pathways with possible negative feedback on ERK signaling and activation of apoptotic pathways (4). These pathways are often conflicting and are context-dependent, indicating a series of self-regulating processes that shift TNFα signaling between cell activation, proliferation, cell survival, apoptosis, cell differentiation, migration and angiogenesis. In the cardiovascular system, TNFα has known inflammatory, vascular permeability, and vasoconstrictor effects (5). TNFα is a robust activator of white blood cells adhesion to endothelial cells through cell adhesion molecules such as VCAM, ICAM and E-selectin (6). TNFα alone does not upregulate endothelial apoptosis, though it may induce apoptosis in conjunction with ceramide-releasing substances and lead to cell death (7). In animal models, TNFα was shown to promote hypertension (8) with local vasoconstriction associated with increased endothelin expression and NFκB-dependent upregulation of endothelin B receptor expression in neighboring smooth muscle cells (9). Administration of the TNFα inhibitor Etanercept in a rat model of PE induced a partial reduction in blood pressure and significantly reduced expression of endothelin-1, suggesting that endothelin-1 expression is at least partially driven by TNFα (10). In addition, TNFα infusion in pregnant rats has shown ~20 mm Hg increase in mean arterial pressure with an increase in endothelin-1 expression in the aorta, placenta, and kidney (11). Consequently, TNFα is considered to be one of the main factors that induce endothelial dysfunction in PE (12).