The Experts below are selected from a list of 21279 Experts worldwide ranked by ideXlab platform
Jeremy J. Mao - One of the best experts on this subject based on the ideXlab platform.
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regenerative endodontics by Cell Homing
Dental Clinics of North America, 2017Co-Authors: Juan Zhong, Jeremy J. Mao, Sahng G Kim, Qimei Gong, Bin Cheng, Junqi LingAbstract:Apical revascularization (AR) and platelet-rich plasma have been used to restore dental pulp vitality in infected immature permanent teeth. Two regenerative therapies are Cell transplantation and Cell Homing. This article updates and benchmarks these therapies with Cell Homing. A case report concluded that AR increased root length; however, quantitative and statistical assessments disproved this. Regenerative endodontic therapies require prospective clinical trials demonstrating safety and efficacy. These therapies are intrinsically susceptible to procedural and patient variations. Cell Homing uses novel molecules that drive therapeutic efficacy, and may be less sensitive to procedural and patient variations.
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dentin and dental pulp regeneration by the patient s endogenous Cells
Endodontic Topics, 2013Co-Authors: Sahng G Kim, Ying Zheng, Jian Zhou, Mo Chen, Mildred C Embree, Karen Song, Nan Jiang, Jeremy J. MaoAbstract:The goal of regenerative endodontics is to restore the functions of the dental pulp–dentin complex. Two approaches are being applied toward dental pulp–dentin regeneration: Cell transplantation and Cell Homing. The majority of previous approaches are based on Cell transplantation by delivering ex vivo cultivated Cells toward dental pulp or dentin regeneration. Many hurdles limit the clinical translation of Cell transplantation such as the difficulty of acquiring and isolating viable Cells, uncertainty of what Cells or what fractions of Cells to use, excessive cost of Cell manipulation and transportation, and the risk of immune rejection, pathogen transmission, and tumorigenesis is associated with ex vivo Cell manipulation. In contrast, Cell Homing relies on induced chemotaxis of endogenous Cells and therefore circumvents many of the difficulties that are associated with Cell transplantation. An array of proteins, peptides, and chemical compounds that are yet to be identified may orchestrate endogenous Cells to regenerate the dental pulp–dentin complex. Both Cell transplantation and Cell Homing are scientifically valid approaches; however, Cell Homing offers a number of advantages that are compatible with the development of clinical therapies for dental pulp–dentin regeneration.
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anatomically shaped tooth and periodontal regeneration by Cell Homing
Journal of Dental Research, 2010Co-Authors: Kwang S Kim, Chang H Lee, B K Kim, Jeremy J. MaoAbstract:Tooth regeneration by Cell delivery encounters translational hurdles. We hypothesized that anatomically correct teeth can regenerate in scaffolds without Cell transplantation. Novel, anatomically shaped human molar scaffolds and rat incisor scaffolds were fabricated by 3D bioprinting from a hybrid of poly-epsilon-caprolactone and hydroxyapatite with 200-microm-diameter interconnecting microchannels. In each of 22 rats, an incisor scaffold was implanted orthotopically following mandibular incisor extraction, whereas a human molar scaffold was implanted ectopically into the dorsum. Stromal-derived factor-1 (SDF1) and bone morphogenetic protein-7 (BMP7) were delivered in scaffold microchannels. After 9 weeks, a putative periodontal ligament and new bone regenerated at the interface of rat incisor scaffold with native alveolar bone. SDF1 and BMP7 delivery not only recruited significantly more endogenous Cells, but also elaborated greater angiogenesis than growth-factor-free control scaffolds. Regeneration of tooth-like structures and periodontal integration by Cell Homing provide an alternative to Cell delivery, and may accelerate clinical applications.
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Regeneration of Dental-Pulp-like Tissue by Chemotaxis-Induced Cell Homing
Tissue engineering. Part A, 2010Co-Authors: Jin Y. Kim, Eduardo K Moioli, Mo Chen, Chang H Lee, Xuejun Xin, Jenny Chung, Peter D. Koch, Jeremy J. MaoAbstract:Tooth infections or injuries involving dental pulp are treated routinely by root canal therapy. Endodontically treated teeth are devitalized, susceptible to re-infections, fractures, and subsequent tooth loss. Here, we report regeneration of dental-pulp-like tissue by Cell Homing and without Cell transplantation. Upon in vivo implantation of endodontically treated real-size, native human teeth in mouse dorsum for the tested 3 weeks, delivery of basic fibroblast growth factor and/or vascular endothelial growth factor (bFGF and/or VEGF) yielded re-Cellularized and revascularized connective tissue that integrated to native dentinal wall in root canals. Further, combined delivery of bFGF, VEGF, or platelet-derived growth factor (PDGF) with a basal set of nerve growth factor (NGF) and bone morphogenetic protein-7 (BMP7) generated Cellularized and vascularized tissues positive of VEGF antibody staining and apparent neo-dentin formation over the surface of native dentinal wall in some, but not all, endodonticall...
Eugene C Butcher - One of the best experts on this subject based on the ideXlab platform.
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role and species specific expression of colon t Cell Homing receptor gpr15 in colitis
Nature Immunology, 2015Co-Authors: Linh P Nguyen, Thanh Theresa Dinh, Husein Hadeiba, Ahmad Ebtikar, Arnulf Hertweck, Richard G Jenner, Edward Ohara, Refik M Gokmen, Graham M Lord, Eugene C ButcherAbstract:The chemoattractant receptor GPR15 can direct CD4+ T Cells to the colon. Habtezion and colleagues show that GATA-3 and Foxp3 exhibit species-specific differences in promoting GPR15 expression and thereby influences Homing of CD4+ effector and regulatory T Cells.
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anti cd43 inhibition of t Cell Homing
Journal of Experimental Medicine, 1997Co-Authors: Leslie M Mcevoy, Hailing Sun, John G Frelinger, Eugene C ButcherAbstract:The Homing of lymphocytes from the blood is controlled by specialized processes of lymphocyte–endothelial Cell interaction. Interference with these processes offers the potential to manipulate lymphocyte traffic, and thus to modulate normal and pathologic immune and inflammatory responses. We selected antilymphocyte monoclonal antibodies (mAbs) for inhibition of lymphocyte binding in vitro to lymph node high endothelial venules (HEV), specialized vessels that support lymphocyte recruitment into lymph nodes. mAb L11 blocks T Cell binding to lymph node and Peyer's patch HEV and inhibits T Cell extravasation from the blood into organized secondary lymphoid tissues. In contrast, L11 has no effect on lymphocyte binding to purified vascular ligands for L-selectin, α4β7, or LFA-1, suggesting that it inhibits by a novel mechanism. The L11 antigen is CD43, a sialomucin implicated in vitro in regulation of lymphocyte activation, whose expression is often dysregulated in the Wiskott-Aldrich syndrome. CD43 represents a novel target for experimental and therapeutic manipulation of lymphocyte traffic and may help regulate T Cell distribution in vivo.
Nikolett Lupsa - One of the best experts on this subject based on the ideXlab platform.
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skin Homing cd8 t Cells preferentially express gpi anchored peptidase inhibitor 16 an inhibitor of cathepsin k
European Journal of Immunology, 2018Co-Authors: Nikolett Lupsa, Barbara Ersek, Andor Horvath, Andras Bencsik, Eszter Lajko, Palma Sillo, Adam Oszvald, Zoltan WienerAbstract:This study sought to identify novel CD8+ T Cell Homing markers by studying acute graft versus host disease (aGvHD), typically involving increased T Cell Homing to the skin and gut. FACS-sorted skin-Homing (CD8β+ /CLA+ ), gut-Homing (CD8β+ /integrinβ7+ ), and reference (CD8β+ /CLA- /integrinβ7- ) T Cells were compared in patients affected by cutaneous and/or gastrointestinal aGVHD. Microarray analysis, qPCR, and flow cytometry revealed increased expression of peptidase inhibitor 16 (PI16) in skin-Homing CD8+ T Cells. Robust association of PI16 with skin Homing was confirmed in all types of aGvHD and in healthy controls, too. PI16 was not observed on CLA+ leukocytes other than T Cells. Induction of PI16 expression on skin-Homing T Cells occurred independently of vitamin D3. Among skin-Homing T Cells, PI16 expression was most pronounced in memory-like CD45RO+ /CD127+ /CD25+ /CD69- /granzyme B- Cells. PI16 was confined to the plasma membrane, was GPI-anchored, and was lost upon restimulation of memory CD8+ T Cells. Loss of PI16 occurred by downregulation of PI16 transcription, and not by Phospholipase C (PLC)- or Angiotensin-converting enzyme (ACE)-mediated shedding, or by protein recycling. Inhibitor screening and pull-down experiments confirmed that PI16 inhibits cathepsin K, but may not bind to other skin proteases. These data link PI16 to skin-Homing CD8+ T Cells, and raise the possibility that PI16 may regulate cutaneous cathepsin K.
Richard G Jenner - One of the best experts on this subject based on the ideXlab platform.
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role and species specific expression of colon t Cell Homing receptor gpr15 in colitis
Nature Immunology, 2015Co-Authors: Linh P Nguyen, Thanh Theresa Dinh, Husein Hadeiba, Ahmad Ebtikar, Arnulf Hertweck, Richard G Jenner, Edward Ohara, Refik M Gokmen, Graham M Lord, Eugene C ButcherAbstract:The chemoattractant receptor GPR15 can direct CD4+ T Cells to the colon. Habtezion and colleagues show that GATA-3 and Foxp3 exhibit species-specific differences in promoting GPR15 expression and thereby influences Homing of CD4+ effector and regulatory T Cells.
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role and species specific expression of colon t Cell Homing receptor gpr15 in colitis
Nature Immunology, 2015Co-Authors: Linh P Nguyen, Thanh Theresa Dinh, Husein Hadeiba, Ahmad Ebtikar, Arnulf Hertweck, Edward Ohara, Refik M Gokmen, Graham M Lord, Junliang Pan, Richard G JennerAbstract:Lymphocyte recruitment maintains intestinal immune homeostasis but also contributes to inflammation. The orphan chemoattractant receptor GPR15 mediates regulatory T Cell Homing and immunosuppression in the mouse colon. We show that GPR15 is also expressed by mouse TH17 and TH1 effector Cells and is required for colitis in a model that depends on the trafficking of these Cells to the colon. In humans GPR15 is expressed by effector Cells, including pathogenic TH2 Cells in ulcerative colitis, but is expressed poorly or not at all by colon regulatory T (Treg) Cells. The TH2 transcriptional activator GATA-3 and the Treg-associated transcriptional repressor FOXP3 robustly bind human, but not mouse, GPR15 enhancer sequences, correlating with receptor expression. Our results highlight species differences in GPR15 regulation and suggest it as a potential therapeutic target for colitis.
Linh P Nguyen - One of the best experts on this subject based on the ideXlab platform.
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role and species specific expression of colon t Cell Homing receptor gpr15 in colitis
Nature Immunology, 2015Co-Authors: Linh P Nguyen, Thanh Theresa Dinh, Husein Hadeiba, Ahmad Ebtikar, Arnulf Hertweck, Richard G Jenner, Edward Ohara, Refik M Gokmen, Graham M Lord, Eugene C ButcherAbstract:The chemoattractant receptor GPR15 can direct CD4+ T Cells to the colon. Habtezion and colleagues show that GATA-3 and Foxp3 exhibit species-specific differences in promoting GPR15 expression and thereby influences Homing of CD4+ effector and regulatory T Cells.
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role and species specific expression of colon t Cell Homing receptor gpr15 in colitis
Nature Immunology, 2015Co-Authors: Linh P Nguyen, Thanh Theresa Dinh, Husein Hadeiba, Ahmad Ebtikar, Arnulf Hertweck, Edward Ohara, Refik M Gokmen, Graham M Lord, Junliang Pan, Richard G JennerAbstract:Lymphocyte recruitment maintains intestinal immune homeostasis but also contributes to inflammation. The orphan chemoattractant receptor GPR15 mediates regulatory T Cell Homing and immunosuppression in the mouse colon. We show that GPR15 is also expressed by mouse TH17 and TH1 effector Cells and is required for colitis in a model that depends on the trafficking of these Cells to the colon. In humans GPR15 is expressed by effector Cells, including pathogenic TH2 Cells in ulcerative colitis, but is expressed poorly or not at all by colon regulatory T (Treg) Cells. The TH2 transcriptional activator GATA-3 and the Treg-associated transcriptional repressor FOXP3 robustly bind human, but not mouse, GPR15 enhancer sequences, correlating with receptor expression. Our results highlight species differences in GPR15 regulation and suggest it as a potential therapeutic target for colitis.