ArticleJournal of neuroinflammation2022
The innate immune receptor Nlrp12 suppresses autoimmunity to the retina.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- Anti-inflammatory mechanisms ofInternational journal of ophthalmology · 2026Article
- Spotlight on pyroptosis: role in pathogenesis and therapeutic potential of ocular diseases.Journal of neuroinflammation · 2022Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundNod-like receptors (NLRs) are critical to innate immune activation and induction of adaptive T cell responses. Yet, their role in autoinflammatory diseases of the central nervous system (CNS) remains incompletely defined. The NLR, Nlrp12, has been reported to both inhibit and promote neuroinflammation in an animal model of multiple sclerosis (experimental autoimmune encephalomyelitis, EAE), where its T cell-specific role has been investigated. Uveitis resulting from autoimmunity of the neuroretina, an extension of the CNS, involves a breach in immune privilege and entry of T cells into the eye. Here, we examined the contribution of Nlrp12 in a T cell-mediated model of uveitis, experimental autoimmune uveitis (EAU).
methodsMice were immunized with interphotoreceptor retinoid-binding protein peptide 1-20 (IRBP
resultsNlrp12
conclusionsOur data identify a combinatorial role for Nlrp12 in dampening autoimmunity of the neuroretina. These findings could provide a pathway for development of therapies for uveitis and potentially other autoinflammatory/autoimmune diseases of the CNS.
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