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Leukocyte migration and graft-versus-host disease
Graft-versus-host disease (GVHD) remains a significant complication of allogeneic bone marrow transplantation (allo-BMT). Acute GVHD is mediated by immunocompetent donor T cells, which migrate to lymphoid tissues soon after infusion, recognize host alloantigens, and become activated upon interaction...
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Published in: | Blood 2005-06, Vol.105 (11), p.4191-4199 |
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creator | Wysocki, Christian A. Panoskaltsis-Mortari, Angela Blazar, Bruce R. Serody, Jonathan S. |
description | Graft-versus-host disease (GVHD) remains a significant complication of allogeneic bone marrow transplantation (allo-BMT). Acute GVHD is mediated by immunocompetent donor T cells, which migrate to lymphoid tissues soon after infusion, recognize host alloantigens, and become activated upon interaction with host antigen-presenting cells (APCs). Recent work from our group and others suggests that activated effector T cells exit lymphoid tissues and traffic to mucosal sites and parenchymal target organs such as the gastrointestinal (GI) tract, liver, lung, and skin where they cause tissue damage. The molecular interactions necessary for effector cell migration during GVHD have become the focus of a growing body of research, as these interactions represent potential therapeutic targets. In this review we discuss chemokine and chemokine receptor interactions and adhesion molecules that have been shown to play roles in effector cell migration in experimental GVHD models, and we discuss a potential model for the role of chemokines during the activation phase of GVHD. |
doi_str_mv | 10.1182/blood-2004-12-4726 |
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Acute GVHD is mediated by immunocompetent donor T cells, which migrate to lymphoid tissues soon after infusion, recognize host alloantigens, and become activated upon interaction with host antigen-presenting cells (APCs). Recent work from our group and others suggests that activated effector T cells exit lymphoid tissues and traffic to mucosal sites and parenchymal target organs such as the gastrointestinal (GI) tract, liver, lung, and skin where they cause tissue damage. The molecular interactions necessary for effector cell migration during GVHD have become the focus of a growing body of research, as these interactions represent potential therapeutic targets. 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Acute GVHD is mediated by immunocompetent donor T cells, which migrate to lymphoid tissues soon after infusion, recognize host alloantigens, and become activated upon interaction with host antigen-presenting cells (APCs). Recent work from our group and others suggests that activated effector T cells exit lymphoid tissues and traffic to mucosal sites and parenchymal target organs such as the gastrointestinal (GI) tract, liver, lung, and skin where they cause tissue damage. The molecular interactions necessary for effector cell migration during GVHD have become the focus of a growing body of research, as these interactions represent potential therapeutic targets. In this review we discuss chemokine and chemokine receptor interactions and adhesion molecules that have been shown to play roles in effector cell migration in experimental GVHD models, and we discuss a potential model for the role of chemokines during the activation phase of GVHD.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Bone marrow, stem cells transplantation. Graft versus host reaction</subject><subject>Cell Adhesion Molecules</subject><subject>Chemokines</subject><subject>Chemotaxis, Leukocyte - physiology</subject><subject>Graft vs Host Disease - etiology</subject><subject>Graft vs Host Disease - immunology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Receptors, Chemokine</subject><subject>Review</subject><subject>Transfusions. Complications. Transfusion reactions. 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Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Bone marrow, stem cells transplantation. Graft versus host reaction</topic><topic>Cell Adhesion Molecules</topic><topic>Chemokines</topic><topic>Chemotaxis, Leukocyte - physiology</topic><topic>Graft vs Host Disease - etiology</topic><topic>Graft vs Host Disease - immunology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Receptors, Chemokine</topic><topic>Review</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wysocki, Christian A.</creatorcontrib><creatorcontrib>Panoskaltsis-Mortari, Angela</creatorcontrib><creatorcontrib>Blazar, Bruce R.</creatorcontrib><creatorcontrib>Serody, Jonathan S.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wysocki, Christian A.</au><au>Panoskaltsis-Mortari, Angela</au><au>Blazar, Bruce R.</au><au>Serody, Jonathan S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leukocyte migration and graft-versus-host disease</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2005-06-01</date><risdate>2005</risdate><volume>105</volume><issue>11</issue><spage>4191</spage><epage>4199</epage><pages>4191-4199</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>Graft-versus-host disease (GVHD) remains a significant complication of allogeneic bone marrow transplantation (allo-BMT). Acute GVHD is mediated by immunocompetent donor T cells, which migrate to lymphoid tissues soon after infusion, recognize host alloantigens, and become activated upon interaction with host antigen-presenting cells (APCs). Recent work from our group and others suggests that activated effector T cells exit lymphoid tissues and traffic to mucosal sites and parenchymal target organs such as the gastrointestinal (GI) tract, liver, lung, and skin where they cause tissue damage. The molecular interactions necessary for effector cell migration during GVHD have become the focus of a growing body of research, as these interactions represent potential therapeutic targets. In this review we discuss chemokine and chemokine receptor interactions and adhesion molecules that have been shown to play roles in effector cell migration in experimental GVHD models, and we discuss a potential model for the role of chemokines during the activation phase of GVHD.</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>15701715</pmid><doi>10.1182/blood-2004-12-4726</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Biological and medical sciences Bone marrow, stem cells transplantation. Graft versus host reaction Cell Adhesion Molecules Chemokines Chemotaxis, Leukocyte - physiology Graft vs Host Disease - etiology Graft vs Host Disease - immunology Humans Medical sciences Receptors, Chemokine Review Transfusions. Complications. Transfusion reactions. Cell and gene therapy |
title | Leukocyte migration and graft-versus-host disease |
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