ArticleInternational journal of hematology2007
Study of relieving graft-versus-host disease by blocking CD137-CD137 ligand costimulatory pathway in vitro.
Article in International journal of hematology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Novel TLR7 agonist stimulates activity of CIK/NK immunological effector cells to enhance antitumor cytotoxicity.Oncology letters · 2018Article
- The Role of Co-stimulatory/Co-inhibitory Signals in Graft-vs.-Host Disease.Frontiers in immunology · 2018Review
- Gene silencing of 4-1BB by RNA interference inhibits acute rejection in rats with liver transplantation.BioMed research international · 2013Article
- T-cell costimulatory molecules in acute-graft-versus host disease: therapeutic implications.Bone marrow research · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Engagement of the TCR without appropriate costimulation will result in the inability of T-cells to respond to the alloantigen as described earlier. We made a further investigation into the effect of relieving graft-versus-host disease (GVHD) and its mechanism in mice by blocking CD137-CD137L pathway in vitro. Responder cells (spleen cells) from BALB/C donor mice (H-2d) were incubated with stimulator cells (spleen cells) from C57BL/6 recipient mice (H-2b), with or without anti-CD137L monoclonal antibodies (MoAbs). Donor bone marrow cells plus mixed lymphocyte culture (MLC) T-cells were transplanted into lethally irradiated C57BL/6 mice. C57BL/6 mice were divided into 3 groups: group A (allogeneic bone marrow transplantation control group), group B (cyclosporine + methotrexate group), and group C (donor T-cells were treated with anti-CD137L MoAbs). The percentage of CD3+CD4+ and CD3+CD8+ T-cells were detected by flow cytometry, and the levels of cytokines (IFN-gamma, interleukin [IL]-2, IL-10, IL-4) by reverse-transcriptase polymerase chain reaction. The incidence of GVHD in group C was 70%, while the incidence of GVHD was 100% in group A and group B. The survival rate of group C was higher than that of group A and B, and the median survival time was longer than that of group A and B (P < .01). Clinical symptoms and histological signs of GVHD in group C were the mildest among all 3 groups. The percentage of CD3+CD8+T-cells in group C was lower than that in group A and B (P < .01). The levels of IFN-gamma in group C were markedly lower than those in group A and B (P < .01), and the levels of IL-10 in group C were significantly higher than those in group A and B (P < .01). The results suggest that treatment of donor T-cells by anti-CD137L MoAbs in vitro may relieve GVHD, thereby improve the survival time and survival rate of recipient mice, which might be related to the increased TH1 cytokine (IFN-gamma) and decreased TH2 cytokine (IL-10) as well as the reduced CD3+CD8+T-cells.
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