ArticleExperimental hematology2007
Factors affecting human T cell engraftment, trafficking, and associated xenogeneic graft-vs-host disease in NOD/SCID beta2mnull mice.
Article in Experimental hematology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 73 citations in OpenAlex.
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- CD4Frontiers in immunology · 2020Article
- Systematic testing and specificity mapping of alloantigen-specific chimeric antigen receptors in regulatory T cells.JCI insight · 2019Article
- Review
- Selective targeting of histone modification fails to prevent graft versus host disease after hematopoietic cell transplantation.PloS one · 2018Article
- Evaluating Human Immune Responses for Vaccine Development in a Novel Human Spleen Cell-Engrafted NOD-SCID-IL2rγNull Mouse Model.Frontiers in immunology · 2018Article
- Article
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Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveGraft-vs-host disease (GVHD) is the major cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation. Models of immunodeficient mice that consistently and efficiently reconstitute with xenoreactive human T cells would be a valuable tool for the in vivo study of GVHD, as well as other human immune responses. MATERIALS AND
methodsWe developed a consistent and sensitive model of human GVHD by retro-orbitally injecting purified human T cells into sublethally irradiated nonobese diabetic/severe combined immunodeficient (NOD/SCID)-beta2m(null) recipients. In addition, we characterized for the first time the trafficking patterns and expansion profiles of xenoreactive human T cells in NOD/SCID-beta2m(null) recipients using in vivo bioluminescence imaging.
resultsAll NOD/SCID-beta2m(null) mice conditioned with 300 cGy total body irradiation and injected with 1 x 10(7) human T cells exhibited human T-cell engraftment, activation, and expansion, with infiltration of multiple target tissues and a subsequent >20% loss of pretransplantation body weight. Importantly, histological examination of the GVHD target tissues revealed changes consistent with human GVHD. Furthermore, we also showed by in vivo bioluminescence imaging that development of lethal GVHD in the NOD/SCID-beta2m(null) recipients was dependent upon the initial retention and early expansion of human T cells in the retro-orbital sinus cavity.
conclusionOur NOD/SCID-beta2m(null) mouse model provides a system to study the pathophysiology of acute GVHD induced by human T cells and aids in development of more effective therapies for human GVHD.
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