ArticleJournal of immunology (Baltimore, Md. : 1950)2013
IL7Rα contributes to experimental autoimmune encephalomyelitis through altered T cell responses and nonhematopoietic cell lineages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Identification and Validation of Biomarkers in the Development and Progression of Graves' Ophthalmopathy.Investigative ophthalmology & visual science · 2026Article
- IL-7Rα on CD4Journal of neuroinflammation · 2024Article
- Aging-related genes revealed Neuroinflammatory mechanisms in ischemic stroke by bioinformatics.Heliyon · 2023Article
- Gene Expression in Spontaneous Experimental Autoimmune Encephalomyelitis Is Linked to Human Multiple Sclerosis Risk Genes.Frontiers in immunology · 2020Article
- Opposing roles of endothelial and leukocyte-expressed IL-7Rα in the regulation of psoriasis-like skin inflammation.Scientific reports · 2019Article
- IL-7-induced phosphorylation of the adaptor Crk-like and other targets.Cellular signalling · 2018Article
- Expression and Regulation of Thymic Stromal Lymphopoietin and Thymic Stromal Lymphopoietin Receptor Heterocomplex in the Innate-Adaptive Immunity of Pediatric Asthma.International journal of molecular sciences · 2018Review
- Down-regulation of interleukin 7 receptor (IL-7R) contributes to central nervous system demyelination.Oncotarget · 2017Article
- Regulation of effector function of CNS autoreactive CD4 T cells through inhibitory receptors and IL-7Rα.Journal of neuroinflammation · 2016Article
- Blockade of CD127 Exerts a Dichotomous Clinical Effect in Marmoset Experimental Autoimmune Encephalomyelitis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016Article
- Interleukin-7 is required for CD4(+) T cell activation and autoimmune neuroinflammation.Clinical immunology (Orlando, Fla.) · 2015Article
- Genetic determinants of risk and progression in multiple sclerosis.Clinica chimica acta; international journal of clinical chemistry · 2015Review
- IL-7/IL-7 Receptor Signaling Differentially Affects Effector CD4+ T Cell Subsets Involved in Experimental Autoimmune Encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Hematogenous macrophage depletion reduces the fibrotic scar and increases axonal growth after spinal cord injury.Neurobiology of disease · 2015Article
- Translational utility of experimental autoimmune encephalomyelitis: recent developments.Journal of inflammation research · 2015Review
- Opposing effects of CTLA4 insufficiency on regulatory versus conventional T cells in autoimmunity converge on effector memory in target tissue.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Transcriptome analysis reveals the contribution of thermal and the specific effects in cellular response to millimeter wave exposure.PloS one · 2014Article
- IL7RA haplotype-associated alterations in cellular immune function and gene expression patterns in multiple sclerosis.Genes and immunity · 2013Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
A mutation in the IL7Rα locus has been identified as a risk factor for multiple sclerosis (MS), a neurodegenerative autoimmune disease characterized by inflammation, demyelination, and axonal damage. IL7Rα has well documented roles in lymphocyte development and homeostasis, but its involvement in disease is largely understudied. In this study, we use the experimental autoimmune encephalomyelitis (EAE) model of MS to show that a less severe form of the disease results when IL7Rα expression is largely restricted to thymic tissue in IL7RTg(IL7R-/-) mice. Compared with wild-type (WT) mice, IL7RTg(IL7R-/-) mice exhibited reduced paralysis and myelin damage that correlated with dampened effector responses, namely decreased TNF production. Furthermore, treatment of diseased WT mice with neutralizing anti-IL7Rα Ab also resulted in significant improvement of EAE. In addition, chimeric mice were generated by bone marrow transplant to limit expression of IL7Rα to cells of either hematopoietic or nonhematopoietic origin. Mice lacking IL7Rα only on hematopoietic cells develop severe EAE, suggesting that IL7Rα expression in the nonhematopoietic compartment contributes to disease. Moreover, novel IL7Rα expression was identified on astrocytes and oligodendrocytes endogenous to the CNS. Chimeric mice that lack IL7Rα only on nonhematopoietic cells also develop severe EAE, which further supports the role of IL7Rα in T cell effector function. Conversely, mice that lack IL7Rα throughout both compartments are dramatically protected from disease. Taken together, these data indicate that multiple cell types use IL7Rα signaling in the development of EAE, and inhibition of this pathway should be considered as a new therapeutic avenue for MS.
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