ArticleInternational immunology2019
RICK/RIP2 is a NOD2-independent nodal point of gut inflammation.
Article in International immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 70 citations in OpenAlex.
- Multiple Modes of Action of Anti-TNF-α Antibodies for Inflammatory Bowel Diseases Beyond TNF-α Neutralization.Antibodies (Basel, Switzerland) · 2026Review
- Nucleotide-binding oligomerization domain 2-independent colonization by Turicimonas muris induced by high-fat diet protects against dextran sodium sulfate-induced colitis.Clinical and experimental immunology · 2026Article
- Clinical description, genetic analysis and characterization of two NLRP12 heterozygous VUS variants.Frontiers in immunology · 2026Article
- Article
- Genotype-phenotype correlation in a cohort of pediatric patients with autoinflammatory diseases carryingFrontiers in immunology · 2025Article
- Current advances on RIPK2 and its inhibitors in pathological processes: a comprehensive review.Frontiers in molecular neuroscience · 2025Review
- RIPK2 Is Crucial for the Microglial Inflammatory Response to Bacterial Muramyl Dipeptide but Not to Lipopolysaccharide.International journal of molecular sciences · 2024Article
- N4BP3 facilitates NOD2-MAPK/NF-κB pathway in inflammatory bowel disease through mediating K63-linked RIPK2 ubiquitination.Cell death discovery · 2024Article
- RIPK2 is crucial for the microglial inflammatory response to bacterial muramyl dipeptide but not to lipopolysaccharide.bioRxiv : the preprint server for biology · 2024Article
- Concurrent occurrence of ulcerative duodenitis and ulcerative colitis displaying unique responses to golimumab and ustekinumab.Clinical journal of gastroenterology · 2024Article
- A positive cytokine/chemokine feedback loop establishes plasmacytoid DC-driven autoimmune pancreatitis in IgG4-related disease.JCI insight · 2024Article
- Reciprocal regulation of protein arginine deiminase 2 and 4 expression in the colonic mucosa of ulcerative colitis.Journal of clinical biochemistry and nutrition · 2024Article
- Specific deletion of Mettl3 in IECs triggers the development of spontaneous colitis and dysbiosis of T lymphocytes in mice.Clinical and experimental immunology · 2024Article
- Circumferential Stenosis of the Second Part of the Duodenum Caused by Eosinophilic Gastroenteritis.Internal medicine (Tokyo, Japan) · 2024Article
- Article
- Crosstalk between NOD2 and TLR2 suppresses the development of TLR2-mediated experimental colitis.Journal of clinical biochemistry and nutrition · 2024Article
- Cytokine and chemokine profiles in ulcerative colitis relapse after coronavirus disease 2019 vaccination.Journal of clinical biochemistry and nutrition · 2024Article
- NOD2-mediated dual negative regulation of inflammatory responses triggered by TLRs in the gastrointestinal tract.Frontiers in immunology · 2024Review
- Role of leucine-rich repeat kinase 2 in severe acute pancreatitis.Frontiers in immunology · 2024Review
- An autopsy case of gas gangrene, massive intravascular hemolysis, and cytokine storm due toIDCases · 2024Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that inhibition of receptor-interacting serine/threonine kinase (RICK) (also known as RIP2) results in amelioration of experimental colitis. This role has largely been attributed to nucleotide-binding oligomerization domain 2 (NOD2) signaling since the latter is considered a major inducer of RICK activation. In this study, we explored the molecular mechanisms accounting for RICK-mediated inhibition of inflammatory bowel disease (IBD). In an initial series of studies focused on trinitrobenzene sulfonic acid (TNBS)-colitis and dextran sodium sulfate (DSS)-colitis we showed that down-regulation of intestinal RICK expression in NOD2-intact mice by intra-rectal administration of a plasmid expressing RICK-specific siRNA was accompanied by down-regulation of pro-inflammatory cytokine responses in the colon and protection of the mice from experimental colitis. Somewhat surprisingly, intra-rectal administration of RICK-siRNA also inhibited TNBS-colitis and DSS-colitis in NOD2-deficient and in NOD1/NOD2-double deficient mice. In complementary studies of humans with IBD we found that expression of RICK, cellular inhibitor of apoptosis protein 2 (cIAP2) and downstream signaling partners were markedly increased in inflamed tissue of IBD compared to controls without marked elevations of NOD1 or NOD2 expression. In addition, the increase in RICK expression correlated with disease activity and pro-inflammatory cytokine responses. These studies thus suggest that NOD1- or NOD2-independenent activation of RICK plays a major role in both murine experimental colitis and human IBD.
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