ReviewInternational immunology2018
Using genes to triangulate the pathophysiology of granulomatous autoinflammatory disease: NOD2, PLCG2 and LACC1.
Review in International immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 35 citations in OpenAlex.
- Integrative gene target mapping, RNA sequencing, in silico molecular docking, ADMET profiling and molecular dynamics simulation study of marine derived molecules for type 1 diabetes mellitus.Molecular diversity · 2026Article
- Combination of mechanical debridement and interleukin 12 or interleukin 23 therapy for refractory facial pyoderma gangrenosum with NOD2 mutation.JAAD case reports · 2025Article
- LACC1 Enhances Polyamine Immunometabolism in Inflammatory Macrophages to Inhibit Atherosclerosis Progression.Journal of cardiovascular translational research · 2025Article
- The research progress of LACC1.Frontiers in immunology · 2025Review
- Causal effects of gut microbiota on sepsis and sepsis-related death: insights from genome-wide Mendelian randomization, single-cell RNA, bulk RNA sequencing, and network pharmacology.Journal of translational medicine · 2024Article
- LACC1 regulates changes in the intestinal flora in a mouse model of inflammatory bowel disease.BMC gastroenterology · 2023Article
- Granulomatous inflammation in inborn errors of immunity.Frontiers in pediatrics · 2023Review
- Article
- Potential Composite Digenic Contribution ofGenes · 2022Article
- [Autoinflammation-A clinical and genetic challenge].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2022Article
- [Autoinflammation-A clinical and genetic challenge].Zeitschrift fur Rheumatologie · 2021Article
- Histologic Patterns and Clues to Autoinflammatory Diseases in Children: What a Cutaneous Biopsy Can Tell Us.Dermatopathology (Basel, Switzerland) · 2021Review
- Four diseases, PLAID, APLAID, FCAS3 and CVID and one gene (PHOSPHOLIPASE C, GAMMA-2;Clinical case reports · 2021Article
- Cell Type Dependent Suppression of Inflammatory Mediators by Myocardin Related Transcription Factors.Frontiers in physiology · 2021Article
- Review
- [Vesicles, pustules and vesiculopustules in early childhood].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2020Article
- NOD1 and NOD2 in inflammatory and infectious diseases.Immunological reviews · 2020Review
- Biochemistry of Autoinflammatory Diseases: Catalyzing Monogenic Disease.Frontiers in immunology · 2019Review
- Novel Molecular Targets Participating in Myocardial Ischemia-Reperfusion Injury and Cardioprotection.Cardiology research and practice · 2019Review
- Introduction: Autoinflammatory Syndromes Special Issue-hidden mysteries in the corners of autoinflammation.International immunology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The intersection of granulomatosis and autoinflammatory disease is a rare occurrence that can be generally subdivided into purely granulomatous phenotypes and disease spectra that are inclusive of granulomatous features. NOD2 (nucleotide-binding oligomerization domain-containing protein 2)-related disease, which includes Blau syndrome and early-onset sarcoidosis, is the prototypic example of granulomatous inflammation in the context of monogenic autoinflammation. Granulomatous inflammation has also been observed in two related autoinflammatory diseases caused by mutations in PLCG2 (phospholipase Cγ2). More recently, mutations in LACC1 (laccase domain-containing protein 1) have been identified as the cause of a monogenic form of systemic juvenile idiopathic arthritis, which does not itself manifest granulomatous inflammation, but the same LACC1 mutations have also been shown to cause an early-onset, familial form of a well-known granulomatous condition, Crohn's disease (CD). Rare genetic variants of PLCG2 have also been shown to cause a monogenic form of CD, and moreover common variants of all three of these genes have been implicated in polygenic forms of CD. Additionally, common variants of NOD2 and LACC1 have been implicated in susceptibility to leprosy, a granulomatous infection. Although no specific mechanistic link exists between these three genes, they form an intriguing web of susceptibility to both monogenic and polygenic autoinflammatory and granulomatous phenotypes.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.