EditorialCrohn's Disease Susceptibility Gene Interactions, a NOD to the Newcomer ATG16L1
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Cited by (22)
Western diet induces Paneth cell defects through microbiome alterations and farnesoid X receptor and type I interferon activation
2021, Cell Host and MicrobeCitation Excerpt :An abnormal Paneth cell phenotype can be driven either by a genetic mutation or by gene-environment interactions (Cadwell et al., 2008, 2010; Kaser et al., 2008; Liu et al., 2013, 2018). While we previously demonstrated that murine norovirus or cigarette smoking could trigger Paneth cell dysfunction in a host with Atg16l1 deficiency (Cadwell, 2010; Liu et al., 2018), the role of persistent viral infection in CD pathogenesis remains elusive (Norman et al., 2015), and abnormal Paneth cell phenotypes can also be found in CD patients who lack ATG16L1 T300A risk alleles or those with a history of cigarette smoking (Liu et al., 2018). Our study of a pediatric CD cohort (of which none were active smokers) showed that an abnormal Paneth cell phenotype is present in ∼50% of CD subjects (Liu et al., 2016), consistent with the results of a previous study showing diminished α-defensins in pediatric CD (Perminow et al., 2010).
Current overview of extrinsic and intrinsic factors in etiology and progression of inflammatory bowel diseases
2014, Pharmacological ReportsCitation Excerpt :NOD2 and ATG16L1 affect dendritic cells and if their functions are impaired, they may cause some shifts in bowel microflora. Interestingly, viral infections may affect ATG16L1 gene expression and increase IBD susceptibility [27], which clearly shows that genetic and environmental factors participate in the pathogenesis of colonic inflammation and its progression. IBD pathogenesis and progression is also associated with mutation in E-cadherin (CDH1) gene [28].
The genetic predisposition and the interplay of host genetics and gut microbiome in crohn disease
2014, Clinics in Laboratory MedicineCitation Excerpt :Genes involved in T-cell circulating, including many specific T-cell subsets, such as T-helper cells (TH17 cells) (STAT3), memory T cells (SP110), and regulatory T cells (STAT5B). Genes in recognition of microbial-associated molecular patterns, including bacterial or fungi sensors NOD1,9 CARD9, NOD2/CARD15,10–17 and toll-like receptors (TLRs). Genes involved in autophagy process, including IRGM, encoding an autophagy protein that plays an important role in innate immunity against intracellular pathogens and CD-associated adherent-invasive Escherichia coli bacteria18–20; ATG16L1, a key component of the autophagy complex that processes and kills intracellular microbes,11,13,17,21 and LRRK2, encoding a complex protein with multiple functional domains, recently found to regulate autophagosome formation through a calcium-dependent pathway.22
NOD2 mutations are associated with the development of intestinal failure in the absence of Crohn's disease
2013, Clinical NutritionCitation Excerpt :Thus, while there was a trend for a higher than expected allele frequency, a true association of the ATG16L1 polymorphism with the development of SBS/IF may have remained undetected in the presence of this high background. b) Along the autophagy pathway ATG16L1 acts down-stream of NOD2.20,21 Thus any NOD2 related pathway may diverge from the CD pathway without the involvement of ATG16L1.
IL-6 effector function of group 2 innate lymphoid cells (ILC2) is NOD2 dependent
2021, Science Immunology
Conflicts of interest The author discloses no conflicts.