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NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn’s disease
by
Rochereau, Nicolas
, Gayet, Rémi
, Paul, Stéphane
, Michaud, Eva
, Roblin, Xavier
, Corthésy, Blaise
, Jospin, Fabienne
, Chanut, Blandine
in
13/1
/ 13/31
/ 13/51
/ 631/250/2152/2153/1291
/ 631/250/256/2515
/ 631/250/347
/ 692/699/1503/257/1402
/ Adaptive immunity
/ Animals
/ Antigen-antibody complexes
/ Colitis - microbiology
/ Colitis - pathology
/ Commensals
/ Crohn Disease - metabolism
/ Crohn Disease - pathology
/ Crohn's disease
/ Digestive system
/ Disease
/ Dysbacteriosis
/ Gastrointestinal tract
/ Gut-associated lymphoid tissues
/ Human health and pathology
/ Humanities and Social Sciences
/ Humans
/ Immunoglobulin A
/ Immunoglobulin A, Secretory - metabolism
/ Immunology
/ Infectious diseases
/ Inflammation
/ Inflammatory bowel diseases
/ Intestinal microflora
/ Intestine
/ Lectins, C-Type - metabolism
/ Life Sciences
/ Lymphoid tissue
/ M cells
/ Mice
/ Mice, Knockout
/ Microbiology and Parasitology
/ Microbiota
/ Models, Biological
/ Mucosa
/ Mucosal immunity
/ multidisciplinary
/ Mutation
/ Mutation - genetics
/ NOD2 protein
/ Nod2 Signaling Adaptor Protein - deficiency
/ Nod2 Signaling Adaptor Protein - genetics
/ Nod2 Signaling Adaptor Protein - metabolism
/ Peyer's Patches - metabolism
/ Pharmaceutical sciences
/ Pharmacology
/ Priming
/ Protein Transport
/ Retrograde transport
/ Salmonella - physiology
/ Science
/ Science (multidisciplinary)
/ Sialic Acid Binding Immunoglobulin-like Lectins - metabolism
/ Transcytosis
/ Translocation
/ Vaccinology
/ Virology
2021
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NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn’s disease
by
Rochereau, Nicolas
, Gayet, Rémi
, Paul, Stéphane
, Michaud, Eva
, Roblin, Xavier
, Corthésy, Blaise
, Jospin, Fabienne
, Chanut, Blandine
in
13/1
/ 13/31
/ 13/51
/ 631/250/2152/2153/1291
/ 631/250/256/2515
/ 631/250/347
/ 692/699/1503/257/1402
/ Adaptive immunity
/ Animals
/ Antigen-antibody complexes
/ Colitis - microbiology
/ Colitis - pathology
/ Commensals
/ Crohn Disease - metabolism
/ Crohn Disease - pathology
/ Crohn's disease
/ Digestive system
/ Disease
/ Dysbacteriosis
/ Gastrointestinal tract
/ Gut-associated lymphoid tissues
/ Human health and pathology
/ Humanities and Social Sciences
/ Humans
/ Immunoglobulin A
/ Immunoglobulin A, Secretory - metabolism
/ Immunology
/ Infectious diseases
/ Inflammation
/ Inflammatory bowel diseases
/ Intestinal microflora
/ Intestine
/ Lectins, C-Type - metabolism
/ Life Sciences
/ Lymphoid tissue
/ M cells
/ Mice
/ Mice, Knockout
/ Microbiology and Parasitology
/ Microbiota
/ Models, Biological
/ Mucosa
/ Mucosal immunity
/ multidisciplinary
/ Mutation
/ Mutation - genetics
/ NOD2 protein
/ Nod2 Signaling Adaptor Protein - deficiency
/ Nod2 Signaling Adaptor Protein - genetics
/ Nod2 Signaling Adaptor Protein - metabolism
/ Peyer's Patches - metabolism
/ Pharmaceutical sciences
/ Pharmacology
/ Priming
/ Protein Transport
/ Retrograde transport
/ Salmonella - physiology
/ Science
/ Science (multidisciplinary)
/ Sialic Acid Binding Immunoglobulin-like Lectins - metabolism
/ Transcytosis
/ Translocation
/ Vaccinology
/ Virology
2021
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NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn’s disease
by
Rochereau, Nicolas
, Gayet, Rémi
, Paul, Stéphane
, Michaud, Eva
, Roblin, Xavier
, Corthésy, Blaise
, Jospin, Fabienne
, Chanut, Blandine
in
13/1
/ 13/31
/ 13/51
/ 631/250/2152/2153/1291
/ 631/250/256/2515
/ 631/250/347
/ 692/699/1503/257/1402
/ Adaptive immunity
/ Animals
/ Antigen-antibody complexes
/ Colitis - microbiology
/ Colitis - pathology
/ Commensals
/ Crohn Disease - metabolism
/ Crohn Disease - pathology
/ Crohn's disease
/ Digestive system
/ Disease
/ Dysbacteriosis
/ Gastrointestinal tract
/ Gut-associated lymphoid tissues
/ Human health and pathology
/ Humanities and Social Sciences
/ Humans
/ Immunoglobulin A
/ Immunoglobulin A, Secretory - metabolism
/ Immunology
/ Infectious diseases
/ Inflammation
/ Inflammatory bowel diseases
/ Intestinal microflora
/ Intestine
/ Lectins, C-Type - metabolism
/ Life Sciences
/ Lymphoid tissue
/ M cells
/ Mice
/ Mice, Knockout
/ Microbiology and Parasitology
/ Microbiota
/ Models, Biological
/ Mucosa
/ Mucosal immunity
/ multidisciplinary
/ Mutation
/ Mutation - genetics
/ NOD2 protein
/ Nod2 Signaling Adaptor Protein - deficiency
/ Nod2 Signaling Adaptor Protein - genetics
/ Nod2 Signaling Adaptor Protein - metabolism
/ Peyer's Patches - metabolism
/ Pharmaceutical sciences
/ Pharmacology
/ Priming
/ Protein Transport
/ Retrograde transport
/ Salmonella - physiology
/ Science
/ Science (multidisciplinary)
/ Sialic Acid Binding Immunoglobulin-like Lectins - metabolism
/ Transcytosis
/ Translocation
/ Vaccinology
/ Virology
2021
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NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn’s disease
Journal Article
NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn’s disease
2021
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Overview
Intestinal microfold cells are the primary pathway for translocation of secretory IgA (SIgA)-pathogen complexes to gut-associated lymphoid tissue. Uptake of SIgA/commensals complexes is important for priming adaptive immunity in the mucosa. This study aims to explore the effect of SIgA retrograde transport of immune complexes in Crohn’s disease (CD). Here we report a significant increase of SIgA transport in CD patients with NOD2-mutation compared to CD patients without
NOD2
mutation and/or healthy individuals. NOD2 has an effect in the IgA transport through human and mouse M cells by downregulating Dectin-1 and Siglec-5 expression, two receptors involved in retrograde transport. These findings define a mechanism of NOD2-mediated regulation of mucosal responses to intestinal microbiota, which is involved in CD intestinal inflammation and dysbiosis.
Trafficking of IgA/commensal complex in the gut has been implicated in inflammatory bowel diseases such as Crohn’s disease, but molecular insights are still lacking. Here the authors show, using mouse model or human cells, that NOD2 mutation increases IgA transport, potentially by altering gut microfold cells from the gut, to impact gut inflammation.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/31
/ 13/51
/ Animals
/ Disease
/ Gut-associated lymphoid tissues
/ Humanities and Social Sciences
/ Humans
/ Immunoglobulin A, Secretory - metabolism
/ Lectins, C-Type - metabolism
/ M cells
/ Mice
/ Microbiology and Parasitology
/ Mucosa
/ Mutation
/ Nod2 Signaling Adaptor Protein - deficiency
/ Nod2 Signaling Adaptor Protein - genetics
/ Nod2 Signaling Adaptor Protein - metabolism
/ Peyer's Patches - metabolism
/ Priming
/ Science
/ Sialic Acid Binding Immunoglobulin-like Lectins - metabolism
/ Virology
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