The effect of NOD2 on the microbiota in Crohn's disease

The effect of NOD2 on the microbiota in Crohn's disease Available online at www.sciencedirect.com ScienceDirect Mackenzie L Lauro, Jason M Burch and Catherine Leimkuhler Grimes Recent advancements toward the treatment of Crohn’s Recognizing this issue, attention has turned to probing disease (CD) indicate great promise for long-term remission. the interactions between the host and microbiome. Ge- CD patients suffer from a complex host of dysregulated netic predisposition is highly correlated to the onset of interactions between their innate immune system and CD. Specifically, mutations to the innate immune recep- microbiome. The most predominant link to the onset of CD is a tor nucleotide-binding oligomerization domain-contain- genetic mutation in the innate immune receptor nucleotide- ing 2 (NOD2) are the strongest genetic factor in the binding oligomerization domain-containing 2 (NOD2). NOD2 advancement of CD and development of an aggressive responds to the presence of bacteria and stimulates the phenotype [3 ]. NOD2 variants contribute to various immune response. Mutations to NOD2 promote low diversity aspects of the pathogenesis. CD patients with NOD2 and dysbiosis in the microbiome, leading to impaired mucosal mutations possess a distinct and compromised microbial barrier function. Current treatments suppress the immune composition that allows harmful bacteria to thrive [4 ]. In response rather than enhancing the function http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Opinion in Biotechnology Elsevier

The effect of NOD2 on the microbiota in Crohn's disease

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Publisher
Elsevier
Copyright
Copyright © 2016 Elsevier Ltd
ISSN
0958-1669
D.O.I.
10.1016/j.copbio.2016.02.028
Publisher site
See Article on Publisher Site

Abstract

Available online at www.sciencedirect.com ScienceDirect Mackenzie L Lauro, Jason M Burch and Catherine Leimkuhler Grimes Recent advancements toward the treatment of Crohn’s Recognizing this issue, attention has turned to probing disease (CD) indicate great promise for long-term remission. the interactions between the host and microbiome. Ge- CD patients suffer from a complex host of dysregulated netic predisposition is highly correlated to the onset of interactions between their innate immune system and CD. Specifically, mutations to the innate immune recep- microbiome. The most predominant link to the onset of CD is a tor nucleotide-binding oligomerization domain-contain- genetic mutation in the innate immune receptor nucleotide- ing 2 (NOD2) are the strongest genetic factor in the binding oligomerization domain-containing 2 (NOD2). NOD2 advancement of CD and development of an aggressive responds to the presence of bacteria and stimulates the phenotype [3 ]. NOD2 variants contribute to various immune response. Mutations to NOD2 promote low diversity aspects of the pathogenesis. CD patients with NOD2 and dysbiosis in the microbiome, leading to impaired mucosal mutations possess a distinct and compromised microbial barrier function. Current treatments suppress the immune composition that allows harmful bacteria to thrive [4 ]. In response rather than enhancing the function

Journal

Current Opinion in BiotechnologyElsevier

Published: Aug 1, 2016

References

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