ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Divergent effects of T cell costimulation and inflammatory cytokine production on autoimmune peripheral neuropathy provoked by Aire deficiency.
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 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Therapeutic options for chronic inflammatory demyelinating polyradiculoneuropathy: a systematic review.BMC neurology · 2014Pooled it
- Age-associated Autoimmunity Driven by T cell Immunosenescence.bioRxiv : the preprint server for biology · 2026Article
- Animal models of immune-mediated demyelinating polyneuropathies.Autoimmunity · 2024Review
- A pathologically expanded, clonal lineage of IL-21-producing CD4+ T cells drives inflammatory neuropathy.The Journal of clinical investigation · 2024Article
- A pathologically expanded, clonal lineage of IL-21 producing CD4+ T cells drives Inflammatory neuropathy.bioRxiv : the preprint server for biology · 2024Article
- An ocular Th1 immune response promotes corneal nerve damage independently of the development of corneal epitheliopathy.Journal of neuroinflammation · 2023Article
- Pathogenic TNF-α drives peripheral nerve inflammation in an Aire-deficient model of autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The NOD Mouse Beyond Autoimmune Diabetes.Frontiers in immunology · 2022Review
- Schwann cell-derived periostin promotes autoimmune peripheral polyneuropathy via macrophage recruitment.The Journal of clinical investigation · 2018Article
- Systemic IGF-1 gene delivery by rAAV9 improves spontaneous autoimmune peripheral polyneuropathy (SAPP).Scientific reports · 2018Article
- IL-10 Paradoxically Promotes Autoimmune Neuropathy through S1PR1-Dependent CD4Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Novel pathomechanisms in inflammatory neuropathies.Journal of neuroinflammation · 2017Review
- Aire-deficient mice provide a model of corneal and lacrimal gland neuropathy in Sjögren's syndrome.PloS one · 2017Article
- Animal models of autoimmune neuropathy.ILAR journal · 2014Review
- Distinct genetic control of autoimmune neuropathy and diabetes in the non-obese diabetic background.Journal of autoimmunity · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chronic inflammatory demyelinating polyneuropathy results from autoimmune destruction of the peripheral nervous system and is a component of the multiorgan autoimmunity syndrome that results from Aire gene mutations in humans. In parallel, peripheral nervous system autoimmunity resembling chronic inflammatory demyelinating polyneuropathy develops spontaneously in NOD mice with a partial loss of Aire function (NOD.Aire(GW/+) mice) and is a T cell-mediated disease. In this study, we analyze how key aspects of T cell activation and function modulate disease development in Aire-deficient mice. We show that genetic ablation of the Th1 cytokine IFN-γ completely prevents clinical and electrophysiological evidence of neuropathy in NOD.Aire(GW/+) mice. IFN-γ deficiency is associated with absence of immune infiltration and decreased expression of the T cell chemoattractant IP-10 in sciatic nerves. Thus, IFN-γ is absolutely required for the development of autoimmune peripheral neuropathy in NOD.Aire(GW/+) mice. Because IFN-γ secretion is enhanced by B7-CD28 costimulation of T cells, we sought to determine the effects of these costimulatory molecules on neuropathy development. Surprisingly, B7-2 deficiency accelerated neuropathy development in NOD.Aire(GW/+) mice, and Ab blockade of both B7-1 and B7-2 resulted in fulminant, early-onset neuropathy. Thus, in contrast to IFN-γ, B7-2 alone and B7-1/B7-2 in combination function to ameliorate neuropathy development in NOD.Aire(GW/+) mice. Together, these findings reveal distinct and opposing effects of the T cell costimulatory pathway and IFN-γ production on the pathogenesis of autoimmune peripheral neuropathy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.