The infusion of ex vivo activated and expanded CD4(+)CD25(+) immune...
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2002 May 15;99(10):3493-9.The infusion of ex vivo activated and expanded CD4(+)CD25(+) immune regulatory cells inhibits graft-versus-host disease lethality.1, , .1University of Minnesota Cancer Center and Department of Pediatrics, Division of Bone Marrow Transplantation, Minneapolis 55455, USA.AbstractImmune regulatory CD4(+)CD25(+) cells play a vital role in the induction and maintenance of self-tolerance and the prevention of autoimmunity. Recently, CD4(+)CD25(+) cells have been shown to be required for the ex vivo induction of tolerance to alloantigen via costimulatory blockade and to inhibit allogeneic skin graft rejection. Data presented here demonstrate that CD4(+)CD25(+) cells play an important role in graft-versus-host disease (GVHD) generation. Depletion of CD4(+)CD25(+) cells from the donor T-cell inoculum or in vivo CD25-depletion of the recipient before transplantation resulted in increased GVHD mediated by CD4(+) or whole T cells in several strain combinations irrespective of the total body irradiation conditioning regime. The infusion of freshly purified donor CD4(+)CD25(+) cells modestly inhibited GVHD when administered in equal numbers with whole CD4(+) cells. Because CD4(+)CD25(+) cells only account for 5% to 10% of the total CD4(+) population, the administration of high numbers of fresh donor CD4(+)CD25(+) cells may not be clinically practical. However, we found that large numbers of CD4(+)CD25(+) cells can be obtained by ex vivo activation and expansion. Cultured CD4(+)CD25(+) cells, administered in equal numbers with CD4(+) T cells or CD25-depleted whole T cells, resulted in significant inhibition of rapidly lethal GVHD. To our knowledge, this study is the first to demonstrate that activated, cultured CD4(+)CD25(+) cells can offer substantial protection in a relevant in vivo animal model of disease. These data have important ramifications for clinical bone marrow and solid organ transplantation. CD4(+)CD25(+) cells warrant consideration as an exciting new modality of cellular therapy for the inhibition of undesirable autologous and allogeneic responses.PMID:
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2004 Feb 15;103(4):1534-41. Epub
2003 Oct 9.Transfer of allogeneic CD62L- memory T cells without graft-versus-host disease.1, , , , .1Bone Marrow Transplantation Program, Department of Medicine, Human Vaccine Institute, Duke University Medical Center, 2400 Pratt St, Ste 1100, Box 3961, Durham, NC 27705, USA.AbstractThe major challenge in allogeneic hematopoietic cell transplantation is how to transfer allogeneic T-cell immunity without causing graft-versus-host disease (GVHD). Here we report a novel strategy to selectively prevent GVHD by depleting CD62L(+) T cells (naive and a subset of memory T cells). In unprimed mice, CD62L(-) T cells (a subset of memory T cells) failed to proliferate in response to alloantigens (which the mice have never previously encountered) and were unable to induce GVHD in allogeneic hosts. CD62L(-) T cells contributed to T-cell reconstitution by peripheral expansion as well as by promoting T-cell regeneration from bone marrow stem/progenitor cells. CD62L(-) T cells from the animals previously primed with a tumor cell line (BCL1) were able to inhibit the tumor growth in vivo but were unable to induce GVHD in the third-party recipients. This novel technology may allow transfer of allogeneic recall antitumor and antimicrobial immunity without causing GVHD.PMID:
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求文献：Acute Graft-vs-Host Disease Development Following Autologous and Syngeneic Bone
1987Acute Graft-vs-Host Disease Development Following Autologous and Syngeneic Bone Marrow TransplantationArch Darchderm:10:745-750. (6). doi.1001&#47
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four patients required systemic corticosteroids to treat their disease, acute cutaneous GVHD was seen in approximately 8% of patients receiving autologous or syngeneic bone marrow transplants at our institution. Ninety-six autologous and 19 syngeneic marrow transplants were performed at our institution between July 1977 and March 1984. Thus. We report acute cutaneous GVHD occurring in seven patients who received autologous marrow and two patients who received marrow from an identical twin. All nine patients had clinically detectable eruptions and had skin biopsy specimens with histologic changes of grade 2 acute GVHD. Although most cases were mild and self-limitingAbstractGraft-vs-host disease (GVHD) is a frequent complication of allogeneic bone marrow transplantation but has been infrequently reported following autologous or syngeneic bone marrow transplantation
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出门在外也不愁Acute graft-versus-host disease: from the bench to the bedside.
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2009 Nov 12;114(20):4327-36. doi: 10.1182/blood-669. Epub
2009 Aug 27.Acute graft-versus-host disease: from the bench to the bedside.1, .1Service d'Hématologie-Greffe, H?pital Saint-Louis, Assistance Publique-Hopitaux de Paris, Université Paris VII Denis-Diderot, and Unité Inserm U728, Paris, France. gerard.socie@sls.aphp.frAbstractDuring the past decade, progress in basic immunology has been impressive. In parallel, whereas our understanding of the pathophysiology of acute graft-versus-host disease (GVHD) has greatly improved, so has our knowledge of the complexities of the immune system. Much of the immunobiology of acute GVHD has been gleaned from preclinical models and far less from correlations with clinical observations or therapeutic interventions. In this review, we summarize some of the major advances in GVHD pathophysiology, including the translation of these from the bench to the bedside, and discuss preclinical approaches that warrant further exploration in the clinic.PMID:
[PubMed - indexed for MEDLINE] PMCID: PMC2777122 Step 1: priming of the immune response. Conditioning regimens used to prepare recipients for allogeneic hematopoietic stem cell transplantation (HSCT) cause graft-versus-host disease (GVHD) parenchymal organ injury and the release of proinflammatory cytokines that initiates allogeneic priming. The red boxes below the mouse and the human recipient serve to highlight distinct features between these species. A major unresolved issue not explained by this schema is shown in the middle red box. RIC denotes reduced-intensity conditioning.Blood. 2009 November 12;114(20):.Step 2: T-cell activation and costimulation. Donor T cells that express positive or inhibitory costimulatory pathway receptors encounter host antigen-presenting cells (APCs) that express major histocompatibility complex (MHC) antigens and ligands for these receptors. A host peptide is shown in the context of MHC/T-cell receptor (TCR) interactions. The red boxes below the mouse and the human recipient serve to highlight distinct features between these species. MiH indicates mino MiHa, minor histoc and Ab, antibody.Blood. 2009 November 12;114(20):.Step 3: regulation of acute GVHD by T-cell subpopulations. T-cell subsets that have been implicated in GVHD generation include naive and effector T cells, and Th1, Th2, and Th17 cells. More uncertain is the role of memory T cells. Inhibitory T-cell populations include CD4+CD25+ regulator T cells and natural killer T cells. In rodents, a T-cell population with stem cell properties has been implicated in acute GVHD generation. The red boxes below the mouse and the human recipient serve to highlight distinct features between these species. Question marks denote uncertain conclusions. Treg indicates T and NKT, natural killer T cell.Blood. 2009 November 12;114(20):.Step 4: T-cell trafficking. In rodents, secondary lymphoid organs are known to facilitate GVHD initiation. In both rodents and humans, GVHD tissue injury requires migration of such activated donor T cells into GVHD target organs that is orchestrated by chemokines, selectin, and adhesion molecules. An example of the homing process into the skin is depicted. The red boxes below the mouse and the human recipient serve to highlight distinct features between these species. Question marks denote uncertain conclusions. In the center red box, we note that clinical translational approaches to prevent GVHD by blocking individual chemokine/receptor interactions may be difficult due to known redundancies that exist for many pathways.Blood. 2009 November 12;114(20):.Step 5: effector phase. Cells implicated in the GVHD effector process are illustrated. In the gray box are the known mediators of tissue injury. IDO inhibits GVHD pathology by reducing the frequency of T-effector cells present in the colon. The red boxes below the mouse and the human recipient serve to highlight distinct features between these species. Question marks denote uncertain conclusions. NK indi TNF, t and TNFa, tumor necrosis factor alpha.Blood. 2009 November 12;114(20):.Publication TypesMeSH TermsGrant SupportFull Text SourcesOther Literature SourcesMiscellaneous
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