ReviewJournal of immunology (Baltimore, Md. : 1950)2025
Resolving the field: a role for Nod2 in T cells.
Review in Journal of immunology (Baltimore, Md. : 1950), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Immunological analysis of Blau syndrome, a unique autoinflammatory state.Frontiers in immunology · 2026Review
- Gut microbiota dysbiosis and immune responses: insights from IgA nephropathy and inflammatory bowel disease.Frontiers in immunology · 2026Review
- Blau syndrome with atrophoderma vermiculata-like appearance: a case report.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
NOD2 is primarily recognized as a cytosolic bacterial sensor of peptidoglycan, activating a downstream Rip2/NF-κB-mediated antimicrobial signaling pathway and playing a vital role in host defense against bacterial infections. NOD2 also appears to play a critical role in immune homeostasis, as NOD2 variants have been linked to multiple human inflammatory diseases, including common polymorphisms that increase the risk of Crohn's disease and rare mutations that cause Blau syndrome. The cellular mechanisms through which mutated NOD2 contributes to disease remain unclear and are currently under investigation. A T cell-intrinsic role for Nod2 in infection and inflammation was suggested almost 15 years ago, leading to intense scrutiny in this research area. This review highlights recent studies establishing a T cell-intrinsic role for NOD2 downstream of T-cell receptor and co-receptor signaling and delineates how NOD2 shapes T-cell responses in both homeostasis and disease, with implications for Blau syndrome and Crohn's disease.
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Identifiers
What Socratic holds
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 Socratic graph.