ArticleImmunity, inflammation and disease2016
Combination treatment with fingolimod and a pathogenic antigen prevents relapse of glucose-6-phosphate isomerase peptide-induced arthritis.
Article in Immunity, inflammation and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Molecular Pharmacology and Novel Potential Therapeutic Applications of Fingolimod.Frontiers in pharmacology · 2022Review
- Treatment approaches to patients with multiple sclerosis and coexisting autoimmune disorders.Therapeutic advances in neurological disorders · 2021Review
- Lactate Buildup at the Site of Chronic Inflammation Promotes Disease by Inducing CD4Cell metabolism · 2019Article
- Immunophenotype and Transcriptome Profile of Patients With Multiple Sclerosis Treated With Fingolimod: Setting Up a Model for Prediction of Response in a 2-Year Translational Study.Frontiers in immunology · 2018Article
- The role of GITR single-positive cells in immune homeostasis.Immunity, inflammation and disease · 2017Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCombination treatment with fingolimod (FTY720) plus pathogenic antigen is thought to prevent glucose-6-phosphate isomerase (GPI)325-339-induced arthritis progression by effective induction of immune tolerance. Here, we examined the efficacy of this combination treatment on remission maintenance.
methodsGPI325-339-induced arthritis mice were treated for 5 days with FTY720 (1.0 mg/kg, p.o.) alone, GPI325-339 (10 μg/mouse, i.v.) alone, or with the FTY720 plus GPI325-339 combination. In some experiments, mice were resensitized with GPI325-339.
resultsFollowing resensitization with GPI325-339, combination-treated mice exhibited neither severe relapse nor elevated lymphocyte infiltration in joints. Neither anti-human nor mouse GPI325-339 antibody levels were correlated with clinical symptoms. This suggests that combination treatment prevents relapse following resensitization via regulation of pathogenic antigen-specific T cells. The proportion of regulatory T (Treg) cells in inguinal lymph nodes was increased post treatment in the FTY720 alone and FTY720 plus GPI325-339 groups. In contrast, the proportion of glucocorticoid-induced tumor necrosis factor receptor-family-related gene/protein (GITR)(+) non-Treg cells was increased only in combination-treated mice. Furthermore, GITR(+) non-Treg cells, which were induced by the combination treatment in vivo, possess suppressive activity and high ability to produce interleukin (IL)-10.
conclusionGITR(+) non-Treg cells might play a key role in relapse prevention following resensitization. Thus, this combination treatment might establish immune tolerance by induction of GITR(+) non-Treg cells.
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