Relevant bibliographies by topics / Host vs Graft Reaction

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Host vs Graft Reaction'

Author: Grafiati
Published: 4 June 2021
Last updated: 27 January 2023

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Journal articles on the topic "Host vs Graft Reaction"

1

Goltz, Robert W. "The Graft-vs-Host Reaction." Archives of Dermatology 124, no. 12 (1988): 1849. http://dx.doi.org/10.1001/archderm.1988.01670120065012.

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Friedman, Kenneth J. "Acute Follicular Graft-vs-Host Reaction." Archives of Dermatology 124, no. 5 (1988): 688. http://dx.doi.org/10.1001/archderm.1988.01670050032014.

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Murphy, William J., Michael Bennett, Miriam R. Anver, Michael Baseler, and Dan L. Longo. "Human-mouse lymphoid chimeras: host-vs.-graft and graft-vs.-host reactions." European Journal of Immunology 22, no. 6 (1992): 1421–27. http://dx.doi.org/10.1002/eji.1830220614.

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Vashisht, Deepak, Rohit Kothari, Sukriti Baveja, Shekhar Neema, Prashant Sengupta, and Sunmeet Sandhu. "Follicular graft Vs host reaction: A rare presentation." Indian Dermatology Online Journal 11, no. 6 (2020): 988. http://dx.doi.org/10.4103/idoj.idoj_87_20.

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Jones, D. C., and N. T. Young. "Natural killer receptors and graft-vs.-host/ graft-vs.-leukaemia reactions." Vox Sanguinis 87, s2 (2004): 15–17. http://dx.doi.org/10.1111/j.1741-6892.2004.00446.x.

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Waer, M., V. Palathumpat, H. Sobis, and M. Vandeputte. "Induction of transplantation tolerance in mice across major histocompatibility barrier by using allogeneic thymus transplantation and total lymphoid irradiation." Journal of Immunology 145, no. 2 (1990): 499–504. http://dx.doi.org/10.4049/jimmunol.145.2.499.

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Abstract The use of allogeneic thymus transplantation as a means of inducing tolerance across MHC barriers was investigated in thymectomized, total lymphoid irradiated BALB/c mice. In 90% of the animals long term outgrowth of histologically normal C57BL thymus grafts was observed. None of the latter animals was chimeric. All thymus graft-bearing mice showed specific nonresponsiveness for C57BL MHC Ag in mixed lymphocyte reaction and cell-mediated lympholysis. Spleen cells of the C57BL thymus-bearing mice were unable to induce lethal graft-vs-host disease in neonatal (BALB/c X C57BL) F1 mice but provoked a vigorous graft-vs-host disease reaction in (BALB/c x C3H) F1 neonates. Tolerant mice permanently accepted C57BL heart and pancreas grafts, but all rejected C3H grafts. Induction of tolerance of BALB/c pre-T cells through allogeneic thymus graft and/or specific suppressor cells seems to be involved. The present model offers new opportunities to study thymocyte maturation in a fully allogeneic environment and may yield applications for clinical organ transplantation.
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Hill, Wolfgang, Karl Sotlar, Heinz Diem, Andreas Hausmann, and Hans Jochem Kolb. "Bone Marrow Reaction in Chronic Graft-Versus-Host Disease." Blood 112, no. 11 (2008): 1166. http://dx.doi.org/10.1182/blood.v112.11.1166.1166.

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Abstract Hematopoiesis of the host is a primary target organ of the graft-versus-host reaction. However histological analyses of the bone marrow are rarely reported. Here we report histological changes in the bone marrow of patients (pts) with and without chronic graft-versus-host disease (cGvHD). Bone marrow biopsies were obtained between 101 days and 4623 days (median:419 days) after transplantation as part of a controlled prospective phase ll study of patients with osteopenia/osteoporosis after allogeneic hematopoietic stem cell transplantation (HCT). Previously we reported an increased density of microvessels using an antibody against v. Willebrand factor (vW) (Hill W. et al Blood110, abstract No 1963; 2007). Here we report additional immunohistological and immunocytological findings in marrow and blood. We analyzed the number of CD34+ and vW+ microvessels as well as CD8+ suppressor/cytotoxic T-cells/mm² (T-S) in sequential biopsies of pts with (n=9) or without (n=6) cGvHD after median 2 years apart. Biopsies of 3 pts without HCT and without lymphoma involvement served as controls. Simultaneously lymphocyte subpopulations were evaluated in peripheral blood samples of pts with (n=16) or without (n=8) cGvHD. The pts were divided in 5 groups: neither aGvHD nor cGvHD; no cGvHD but acute GvHD before entry; cGvHD limited; cGvHD extensive without immunosuppression; cGvHD extensive with immunosuppression. Results: In the first biopsies the content of CD34+, vW+ microvessels and T-S cells were significantly higher in pts with cGvHD (group 3–5) than in those without cGvHD (group 1–2) (21,3 vs 8,2 p=0,03; 22,0 vs 9,2 p=0,002 respectively 106,2 vs 32,1 p=0,04). In the second biopsies these parameters were also increased in cGvHD: CD34+ (18,3 vs 11,2 p=0,02), vW+ (17,3 vs 9,0 p=0,08) microvessels and T-S cells (63,2 vs 37,8 p=0,27). The increased density of CD34+ and vW+ microvessels correlated with the number of T-S cells (p=0,05). As compared to normal controls we observed a significantly higher content of vW+ microvessels in all groups of transplanted pts (16,9 vs 4,2 p=0,03). In pts with cGvHD (group 3–5) CD34+ and vW+ microvessels were further increased (p=0,02 respectively p=0,002). At the time of the first biopsy the absolute T-S cell content in peripheral blood was moderately increased in group 5 (1124/ul) and minimally increased in group 2 (993/ul) (normal 270 – 880), whereas the overall T cell (CD3) content was normal in all groups. The percentage of activated T-S (HLA-DR+) cells was increased in all groups of transplanted pts (61,8% vs normal =33%; p=0,05). After two years T-S cells content was reduced in pts under immunosuppressive therapy (group 5) (1415 vs 900/ul; p=0.000) but remained increased over the norm. In group 4 T-S cell content was increased over the norm (800 vs 920/ul; p=0,043). In conclusion, sequential immunohistology and immunocytology analyses on bone marrow biopsies and peripheral blood provide evidence for the existence of a chronic graft-versus-host reaction of the bone marrow in pts with cGvHD. This is characterized by an increased content of CD34+ and vW+ microvessels and an increased content of T-S cells at least initially. However this reaction does not lead to a generalized hematopoietic insufficiency.
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Friedman, K. J. "Acute follicular graft-vs-host reaction. A distinct clinicopathologic presentation." Archives of Dermatology 124, no. 5 (1988): 688–91. http://dx.doi.org/10.1001/archderm.124.5.688.

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Hakim, F. T., S. Payne, and G. M. Shearer. "Recovery of T cell populations after acute graft-vs-host reaction." Journal of Immunology 152, no. 1 (1994): 58–64. http://dx.doi.org/10.4049/jimmunol.152.1.58.

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Abstract We previously have observed that T dependent immune functions were deficient for several months after induction of acute suppressive graft-vs-host-reaction (GVHR) by injection of parental C57BL/10 donor spleen cells into unirradiated (B10 x B10.BR) F, hosts. We therefore investigated whether new T cells matured after acute GVHR, and whether these were tolerant of host Ag. By 8 to 17 mo after GVHR, the frequencies of splenic CD4 and CD8 T cells were found to be comparable to age-matched untreated hosts, although the lymphoid organ size and hence the total number of T cells was significantly reduced. When GVHR was induced with a combination of C57BL/6 (Thy-1.2) mature lymphocytes and B6.PL (Thy-1.1) bone marrow stem cells, the mature donor Thy-1.2 T cells initially predominated during the acute GVHR. After several months, however, 75% of the CD4 and 50% of the CD8 T cell population was derived from donor Thy-1.1% pre-T cells that had matured in the host. Long term GVHR spleen cells were unresponsive to host Ag in CTL assays, but did not suppress anti-host CTL responses. Finally, host-reactive V beta 11 TCR expressing cells were found to be clonally deleted from splenic CD4 and CD8 populations, consistent with intrathymic negative selection. This evidence suggests that the post-GVHR thymus has the capacity to produce and negatively select phenotypically mature CD4 and CD8 T cells and that a failure to clonally delete self-reactive populations is not a contributing factor to the development of chronic GVHR in this system.
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Pals, S. T., M. Zijstra, T. Radaszkiewicz, et al. "Immunologic induction of malignant lymphoma: graft-vs-host reaction-induced B cell lymphomas contain integrations of predominantly ecotropic murine leukemia proviruses." Journal of Immunology 136, no. 1 (1986): 331–39. http://dx.doi.org/10.4049/jimmunol.136.1.331.

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Abstract The induction of a graft-vs-host reaction in (BALB/c X A)F1 mice by i.v. injection with BALB/c lymphoid cells leads to a lymphoid hyperplasia that may progress to malignant lymphoma. In the present paper, the following aspects of graft-vs-host-reaction lymphomagenesis were studied: 1) the cellular requirements for the induction of lymphomas, 2) their cellular origin, and 3) the role of murine leukemia viruses. The development of graft-vs-host-reaction lymphomas was found to be mediated by donor T cells and to require the presence of histoincompatibility between donor and host. Histologically, the vast majority of these lymphomas were either of follicular center cell or of immunoblastic type, whereas immunoperoxidase studies showed that they were virtually all B cell derived. Most of the lymphomas were of host origin. In the DNA of approximately 80% of the lymphomas, integrated murine leukemia virus proviruses were detected. In the B cell lymphoma DNA, integrated ecotropic proviruses prevailed, but recombinant murine leukemia virus and/or deleted murine leukemia virus genomes were also detected in some tumor DNA.
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Dissertations / Theses on the topic "Host vs Graft Reaction"

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King, Marie A. "The Humanized Mouse Model: The Study of the Human Alloimmune Response: A Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/374.

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The transplantation of allogeneic cells and tissues for the treatment of human disease has been a life-saving procedure for many thousands of patients worldwide. However, to date, neither solid organ transplantation nor bone marrow transplantation have reached their full clinical potential. Significant limitations to the advancement of clinical transplantation stem from our current inability to prevent the rejection of allogeneic tissues by the immune system of the host. Similarly, in patients that receive allogeneic bone marrow transplants, we cannot permanently prevent the engrafted immune system from mounting a response against the patient. This problem, termed graft versus host disease is the most prevalent cause of morbidity and mortality in recipients of allogeneic bone marrow transplants. Clinically, we rely on lifelong immunosuppression to prolong survival of allogeneic tissues within the host. Our currently available therapeutics burden patients with side-effects that range from being unpleasant to life-threatening, while in most cases offering only a temporary solution to the problem of alloimmunity. Efforts are underway to develop protocols and therapeutics that more effectively prevent the pathology associated with alloimmunity. To minimize patient risk, extensive pre-clinical studies in laboratory animals are conducted to predict clinical responses. In the case of immunologic studies, many of these pre-clinical studies are carried out in murine models. Unfortunately, studies of murine immunity often do not predict outcomes in the clinic. One approach to overcome this limitation is the development of a small animal model of the human immune system. In this dissertation, we hypothesized that NOD-scid IL2rγnull mice engrafted with human peripheral blood mononuclear cells (PBMC), termed the hu-PBMC-NOD-scid IL2rγnull model, would provide a model that more accurately reflects human immunity in vivo than other models currently available. To investigate this possibility, we first investigated whether NOD-scid IL2rγnull mice were able to support the engraftment of human PBMC. We found that NOD-scid IL2rγnull mice engraft with human PBMC at much higher levels then the previous gold standard model, the NOD-scid mouse. We then investigated the kinetics of human cell engraftment, determined the optimal cell dose, and defined the influence of injection route on engraftment levels. Even at low PBMC input, NOD-scid IL2rγnullmice reproducibly support high levels of human PBMC engraftment. In contrast to previous stocks of immunodeficient mice, we observed low intra- and interdonor variability of engraftment. We next hypothesized that the human PBMC engrafted in NOD-scid IL2rγnull mice were functional and would reject transplanted allogeneic human tissues. To test this, human islets were transplanted into the spleen of chemically diabetic NOD-scid IL2rγnull mice with or without intravenous injection of HLA-mismatched human PBMC. In the absence of allogeneic PBMC, the human islets were able to restore and maintain normoglycemia. In contrast, human islet grafts were completely rejected following injection of HLA-mismatched human PBMC as evidenced by return to hyperglycemia and loss of human C-peptide in the circulation. Thus, PBMC engrafted NOD-scid IL2rγnull mice are able to provide an in vivomodel of a functional human immune system and of human islet allograft rejection. The enhanced ability of NOD-scid IL2rγnull mice to support human cell engraftment gave rise to the possibility of creating a model of graft versus host disease mediated by a human immune system. To investigate this possibility, human PBMC were injected via the tail vein into lightly irradiated NOD-scid IL2rγnull mice. We found that in contrast to previous models of GVHD using human PBMC-injected immunodeficient mice, these mice consistently (100%) developed GVHD following injection of as few as 5x106PBMC, regardless of the PBMC donor used. We then tested the contribution of host MHC in the development of GVHD in this model. As in the human disease, the development of GVHD was highly dependent on host expression of MHC class I and class II molecules. To begin to evaluate the extent to which the PBMC-engrafted NOD-scid IL2rγnull humanized mouse model of GVHD represents the clinical disease, we tested the ability of a therapeutic in clinical trials to modulate GVHD in these mice. In agreement with the clinical experience, we found that interrupting the TNFα signaling cascade with etanercept delayed the onset and severity of disease in this model. In summary, we conclude that humanized NOD-scid IL2rγnull mice represent an important surrogate for investigating in vivo mechanisms of both human islet allograft rejection and graft versus host disease.
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Watret, Karen Christine. "Graft-versus-host reaction and the mucosal immune response." Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/19395.

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Carlens, Stefan. "Leukaemic relapse after allogeneic haematopoietic stem cell transplantation and the use of the graft-versus-leukaemia effect /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4310-9/.

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Desbarats, Julie. "Mechanisms of T cell immunosuppression during the graft-versus-host reaction." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28728.

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The studies presented in this thesis examine the mechanisms of T cell immunosuppression during the graft-versus-host reaction (GVHR). GVHR was induced by the injection of parental lymphoid cells into F1 hybrid recipient mice. The ensuing acute reaction consisted of an initial immunoproliferative phase, followed by the development of profound immunosuppression and histopathological lesions of epithelial and lymphoid tissues. Survivors of the acute reaction developed the persistent immune abnormalities characteristic of chronic GVHR.<br>We have found that the T cell protein tyrosine kinases p56$ rm sp{lck}$ and p59$ rm sp{fyn}$, involved in signal transduction through the T cell receptor (TCR), are downregulated in the T cells of mice during GVHR. The reduction of lck and fyn was prevented by adrenalectomy of the recipients, and a similar reduction could be induced in normal (non-GVH-reactive) mice by an injection of exogenous cortisone. These findings suggested that the GVHR-induced elevation in endogenous glucocorticoid levels could trigger the decrease of T cell lck and fyn, resulting in a T cell signalling defect during GVHR. In fact, we have demonstrated that glucocorticoids induced a decrease in lck and fyn in T cell clones in vitro. Thus, it appeared that the early GVHR-induced T cell unresponsiveness was due to the glucocorticoid-dependent downregulation of T cell lck and fyn.<br>We have investigated changes in T cell maturation and selection in the GVHR-dysplastic thymus, which may account for the persistent immune abnormalities of chronic GVHR. Thymocyte TCR expression and usage were aberrant during GVHR; changes included decreased expression of CD3 on CD4$ sp+$8 thymocytes, inconsistent TCR V$ beta$ usage, and appearance of phenotypically autoreactive mature thymocytes. These abnormalities, suggestive of defective positive and negative selection, are likely to result from the GVHR-induced decrease in thymic class II MHC expression. Altered T cell education may lead to the long-term peripheral T cell defects observed in chronic GVHR. Lastly, we report that GVHR-induced cutaneous injury was exacerbated by irradiation of the target tissue, suggesting that in clinical GVHR, irradiation may intensify tissue damage, including thymic epithelial lesions; this could potentially lead to more serious alterations in thymic function, and thus to longer lasting, more severe peripheral T cell immune deficiency.
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Peres, Amos. "Effects of an interferon inducer, pI:C, on the graft-versus-host reaction." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74294.

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Polyinosinic: polycytidylic acid (pI:C), an interferon (IFN) inducer, was used to investigate the role of IFN in the graft-versus-host reaction (GVHR), induced by injecting parental cells into F1 recipients and assessed for immunosuppression and pathological lesions.<br>PI:C-treatment of recipients, but not donors, before GVHR-induction suppressed the GVHR, an effect seen only with C57BL/6 (B6) and not A donor cells. Using fluorescein-labelled donor cells, pI:C-treatment was seen to cause a marked decrease in donor cell survival after 2 days. Elimination of donor cells was specific for the B6 donor, was associated with increased natural killer (NK) cell but not macrophage cytotoxic activity, was radioresistant and anti-asialo GM1 sensitive, evidence supporting NK-mediated rejection.<br>Plotting donor cell recovery against the number of cells injected into variously treated recipients indicated that in unstimulated mice a constant proportion of the injected cells were rejected, pI:C increasing that proportion, suggesting that pI:C changes F1 NK target repertoire.<br>PI:C-treatment after GVHR-induction increased the severity of the GVHR, especially soon after GVHR-induction, the effect waning afterwards. No strain dependence was observed.<br>These results demonstrate that IFN/IFN-activated cells play an important role in the regulation and in the immunosuppression/pathogenesis of a GVHR.
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Jaksch, Marie. "Molecular monitoring of acute graft-versus-host disease after allogeneic stem cell transplantation /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-987-0/.

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Li, Hu [Verfasser]. "Mechanisms of Glucocorticoids in the modulation of Graft-versus-Host Disease and the Graft-versus-Leukemia Reaction / Hu Li." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2020. http://d-nb.info/1215338570/34.

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Rotolo, Jimmy A. "Ceramide-mediated platform generation regulates apoptosis in vitro and in vivo /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1428842781&sid=10&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Svahn, Britt-Marie. "Stem cell transplantation: home care, graft-versus-host disease and costs /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-611-5/.

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Ghimire, Sakhila [Verfasser], and Ernst [Akademischer Betreuer] Holler. "Analysis of the Immune Cell Infiltrates and Biomarkers during acute Gastrointestinal Graft vs Host Disease / Sakhila Ghimire ; Betreuer: Ernst Holler." Regensburg : Universitätsbibliothek Regensburg, 2016. http://d-nb.info/1122355769/34.

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Books on the topic "Host vs Graft Reaction"

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M, Ferrara James L., Deeg H. Joachim, and Burakoff Steven J, eds. Graft-vs.-host disease. 2nd ed. Marcel Dekker, 1996.

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Julian, Verbov, ed. Talking points in dermatology--I. MTP Press, 1986.

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R, Forsythe John L., ed. Transplantation surgery: Current dilemmas. 2nd ed. W. B. Saunders, 2001.

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Ferrara, James L. M., 1952-, Cooke Kenneth R, and Deeg H. Joachim 1945-, eds. Graft-vs.-host disease. 3rd ed. Marcel Dekker, 2005.

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Yeung, Cecilia C. S., and Howard M. Shulman, eds. Pathology of Graft vs. Host Disease. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-42099-8.

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Chao, Nelson J. Graft-versus-host disease. R.G. Landes Co., 1994.

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Chao, Nelson J. Graft-versus-host-disease. 2nd ed. R.G. Landes Co., 1999.

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Symposium in Immunology (1st 1991?). Symposium in Immunology I, Symposium in Immunology II. Springer-Verlag, 1993.

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1947-, Kurtz Stanford R., Baldwin Michael L, and Sirchia Girolamo, eds. Controversies in transfusion medicine: Immune complications and cytomegalovirus transmission. American Association of Blood Banks, 1990.

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J, Cant Andrew, Galloway Angela, and Jackson Graham FRCP, eds. Practical hematopoietic stem cell transplantation. Blackwell Pub., 2007.

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Book chapters on the topic "Host vs Graft Reaction"

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Müller-Hermelink, H. K., and E. Deltz. "Graft-vs-Host Reaction After Small-Bowel Transplantation Compared with Graft-vs-Host Reaction After Bone Marrow Transplantation." In Small-Bowel Transplantation. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71087-2_24.

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Ferguson, A., A. G. Cummins, G. H. Munro, and S. Gibson. "Mucosal Mast Cells in Experimental Graft-vs-Host Reaction." In Small-Bowel Transplantation. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71087-2_22.

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Ferguson, A., and A. G. Cummins. "Early Intestinal Lesions of Graft-vs-Host Reaction and Allograft Rejection in Rodents, Identified by Quantitative Histological Techniques." In Small-Bowel Transplantation. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71087-2_21.

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Spitzer, Thomas R., and Robert Sackstein. "Graft-vs-Host Disease." In Current Controversies in Bone Marrow Transplantation. Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-657-7_17.

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Holsapple, Michael. "Graft-Versus-Host Reaction." In Encyclopedia of Immunotoxicology. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_624.

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Timson, David J., Richard J. Reece, James B. Thoden, et al. "Graft Versus Host Reaction." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8651.

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Shustov, Andrei, Violetta Rus, Phuong Nguyen, and Charles S. Via. "Murine Graft-vs-Host Disease." In Lupus. Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-703-1_9.

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Platzbecker, Uwe, and H. Joachim Deeg. "Acute Graft-vs-Host Disease." In Stem Cell Transplantation for Hematologic Malignancies. Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-733-8_7.

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Ho, Min Kin Derek, and Noah Scheinfeld. "Graft vs Host Disease and Skin Manifestations." In Skin Diseases in the Immunocompromised. Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6479-1_6.

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Goldstein, Steven C., Sophie D. Stein, and David L. Porter. "Treatment of Acute Graft-vs-Host Disease." In Allogeneic Stem Cell Transplantation. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-478-0_42.

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Conference papers on the topic "Host vs Graft Reaction"

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Perobelli, Suelen Martins, Ana Carolina Terra Mercadante, Triciana Gonçalves-Silva, et al. "Abstract B39: Neutrophils G-CSF stimulated promotes specific protection against graft vs. host disease and keeps the graft vs. leukemia effect." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b39.

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Ahle, D., B. McDaniel, M. B. Grisham, and S. Almodovar. "Graft vs Host Disease Is Not Associated with HIV-Mediated Pulmonary Smooth Muscle Hypertrophy in Humanized Mice." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5036.

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Nohra, C., H. Ota, J. K. Y. Wu, et al. "Lung Function Monitoring in Patients with Pulmonary Graft vs. Host Disease Following Bone Marrow Transplantation (BMT) Using Oscillometry." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1048.

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Reports on the topic "Host vs Graft Reaction"

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Gelb, Jr., Jack, Yoram Weisman, Brian Ladman, and Rosie Meir. Identification of Avian Infectious Brochitis Virus Variant Serotypes and Subtypes by PCR Product Cycle Sequencing for the Rational Selection of Effective Vaccines. United States Department of Agriculture, 2003. http://dx.doi.org/10.32747/2003.7586470.bard.

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Objectives 1. Determine the serotypic identities of 40 recent IBV isolates from commercial chickens raised in the USA and Israel. 2. Sequence all IBV field isolates using PCR product cycle sequencing and analyze their S 1 sequence to detennine their homology to other strains in the Genbank and EMBL databases. 3. Select vaccinal strains with the highest S 1 sequence homology to the field isolates and perform challenge of immunity studies in chickens in laboratory trials to detennine level of protection afforded by the vaccines. Background Infectious bronchitis (IB) is a common, economically important disease of the chicken. IB occurs as a respiratory form, associated with airsacculitis, condemnation, and mortality of meat-type broilers, a reproductive form responsible for egg production losses in layers and breeders, and a renal form causing high mortality in broilers and pullets. The causative agent is avian coronavirus infectious bronchitis virus (IBV). Replication of the virus' RNA genome is error-prone and mutations commonly result. A major target for mutation is the gene encoding the spike (S) envelope protein used by the virus to attach and infect the host cell. Mutations in the S gene result in antigenic changes that can lead to the emergence of variant serotypes. The S gene is able to tolerate numerous mutations without compromising the virus' ability to replicate and cause disease. An end result of the virus' "flexibility" is that many strains of IBV are capable of existing in nature. Once formed, new mutant strains, often referred to as variants, are soon subjected to immunological selection so that only the most antigenically novel variants survive in poultry populations. Many novel antigenic variant serotypes and genotypes have been isolated from commercial poultry flocks. Identification of the field isolates of IBV responsible for outbreaks is critical for selecting the appropriate strain(s) for vaccination. Reverse transcriptase polymerase chain reaction (RT-PCR) of the Sl subunit of the envelope spike glycoprotein gene has been a common method used to identify field strains, replacing other time-consuming or less precise tests. Two PCR approaches have been used for identification, restriction fragment length polymorphism (RFLP) and direct automated cycle sequence analysis of a diagnostically relevant hypervariab1e region were compared in our BARD research. Vaccination for IB, although practiced routinely in commercial flocks, is often not protective. Field isolates responsible for outbreaks may be unrelated to the strain(s) used in the vaccination program. However, vaccines may provide varying degrees of cross- protection vs. unrelated field strains so vaccination studies should be performed. Conclusions RFLP and S1 sequence analysis methods were successfully performed using the field isolates from the USA and Israel. Importantly, the S1 sequence analysis method enabled a direct comparison of the genotypes of the field strains by aligning them to sequences in public databases e.g. GenBank. Novel S1 gene sequences were identified in both USA and Israel IBVs but greater diversity was observed in the field isolates from the USA. One novel genotype, characterized in this project, Israel/720/99, is currently being considered for development as an inactivated vaccine. Vaccination with IBV strains in the US (Massachusetts, Arkansas, Delaware 072) or in Israel (Massachusetts, Holland strain) provided higher degrees of cross-protection vs. homologous than heterologous strain challenge. In many cases however, vaccination with two strains (only studies with US strains) produced reasonable cross-protection against heterologous field isolate challenge. Implications S1 sequence analysis provides numerical similarity values and phylogenetic information that can be useful, although by no means conclusive, in developing vaccine control strategies. Identification of many novel S1 genotypes of IBV in the USA is evidence that commercial flocks will be challenged today and in the future with strains unrelated to vaccines. In Israel, monitoring flocks for novel IBV field isolates should continue given the identification of Israel/720/99, and perhaps others in the future. Strains selected for vaccination of commercial flocks should induce cross- protection against unrelated genotypes. Using diverse genotypes for vaccination may result in immunity against unrelated field strains.
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