NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells

NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells

NLRs (nucleotide-binding domain leucine-rich repeat containing receptors; NOD-like receptors) are a class of pattern recognition receptor (PRR) that respond to host perturbation from either infectious agents or cellular stress1,2. The function of most NLR family members has not been characterized an...

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Main Authors: Eisenbarth, Stephanie C., Williams, Adam, Colegio, Oscar R., Meng, Hailong, Strowig, Till, Rongvaux, Anthony, Henao-Mejia, Jorge, Thaiss, Christoph A., Joly, Sophie, Gonzalez, David, Xu, Lan, Zenewicz, Lauren A., Haberman, Ann M., Elinav, Eran, Kleinstein, Steven H., Sutterwala, Fayyaz S., Flavell, Richard A.
Format: Online
Language:English
Published: 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3340615/
id pubmed-3340615
recordtype oai_dc
spelling pubmed-33406152012-10-26 NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells Eisenbarth, Stephanie C. Williams, Adam Colegio, Oscar R. Meng, Hailong Strowig, Till Rongvaux, Anthony Henao-Mejia, Jorge Thaiss, Christoph A. Joly, Sophie Gonzalez, David Xu, Lan Zenewicz, Lauren A. Haberman, Ann M. Elinav, Eran Kleinstein, Steven H. Sutterwala, Fayyaz S. Flavell, Richard A. Article NLRs (nucleotide-binding domain leucine-rich repeat containing receptors; NOD-like receptors) are a class of pattern recognition receptor (PRR) that respond to host perturbation from either infectious agents or cellular stress1,2. The function of most NLR family members has not been characterized and their role in instructing adaptive immune responses remains unclear 2,3. NLRP10 (also known as PYNOD, NALP10, PAN5 and NOD8) is the only NLR lacking the putative ligand binding leucine rich repeat domain, and has been postulated to be a negative regulator of other NLR members including NLRP34–6. We did not find evidence that NLRP10 functions through an inflammasome to regulate caspase-1 activity nor that it regulates other inflammasomes. Instead, Nlrp10−/− mice had a profound defect in helper T cell-driven immune responses to a diverse array of adjuvants including lipopolysaccharide (LPS), aluminium hydroxide (alum) and complete Freund’s adjuvant (CFA). Adaptive immunity was impaired in the absence of NLRP10 due to a dendritic cell (DC) intrinsic defect in emigration from inflamed tissues while upregulation of DC costimulatory molecules and chemotaxis to CCR7-dependent and independent ligands remained intact. The loss of antigen transport to the draining LN by this migratory DC subset resulted in an almost absolute loss in naïve CD4+ T cell priming, highlighting the critical link between diverse innate immune stimulation, NLRP10 activity and the immune function of mature DCs. 2012-04-25 /pmc/articles/PMC3340615/ /pubmed/22538615 http://dx.doi.org/10.1038/nature11012 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Eisenbarth, Stephanie C.
Williams, Adam
Colegio, Oscar R.
Meng, Hailong
Strowig, Till
Rongvaux, Anthony
Henao-Mejia, Jorge
Thaiss, Christoph A.
Joly, Sophie
Gonzalez, David
Xu, Lan
Zenewicz, Lauren A.
Haberman, Ann M.
Elinav, Eran
Kleinstein, Steven H.
Sutterwala, Fayyaz S.
Flavell, Richard A.
spellingShingle Eisenbarth, Stephanie C.
Williams, Adam
Colegio, Oscar R.
Meng, Hailong
Strowig, Till
Rongvaux, Anthony
Henao-Mejia, Jorge
Thaiss, Christoph A.
Joly, Sophie
Gonzalez, David
Xu, Lan
Zenewicz, Lauren A.
Haberman, Ann M.
Elinav, Eran
Kleinstein, Steven H.
Sutterwala, Fayyaz S.
Flavell, Richard A.
NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells
author_facet Eisenbarth, Stephanie C.
Williams, Adam
Colegio, Oscar R.
Meng, Hailong
Strowig, Till
Rongvaux, Anthony
Henao-Mejia, Jorge
Thaiss, Christoph A.
Joly, Sophie
Gonzalez, David
Xu, Lan
Zenewicz, Lauren A.
Haberman, Ann M.
Elinav, Eran
Kleinstein, Steven H.
Sutterwala, Fayyaz S.
Flavell, Richard A.
author_sort Eisenbarth, Stephanie C.
title NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells
title_short NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells
title_full NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells
title_fullStr NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells
title_full_unstemmed NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells
title_sort nlrp10 is a nod-like receptor essential to initiate adaptive immunity by dendritic cells
description NLRs (nucleotide-binding domain leucine-rich repeat containing receptors; NOD-like receptors) are a class of pattern recognition receptor (PRR) that respond to host perturbation from either infectious agents or cellular stress1,2. The function of most NLR family members has not been characterized and their role in instructing adaptive immune responses remains unclear 2,3. NLRP10 (also known as PYNOD, NALP10, PAN5 and NOD8) is the only NLR lacking the putative ligand binding leucine rich repeat domain, and has been postulated to be a negative regulator of other NLR members including NLRP34–6. We did not find evidence that NLRP10 functions through an inflammasome to regulate caspase-1 activity nor that it regulates other inflammasomes. Instead, Nlrp10−/− mice had a profound defect in helper T cell-driven immune responses to a diverse array of adjuvants including lipopolysaccharide (LPS), aluminium hydroxide (alum) and complete Freund’s adjuvant (CFA). Adaptive immunity was impaired in the absence of NLRP10 due to a dendritic cell (DC) intrinsic defect in emigration from inflamed tissues while upregulation of DC costimulatory molecules and chemotaxis to CCR7-dependent and independent ligands remained intact. The loss of antigen transport to the draining LN by this migratory DC subset resulted in an almost absolute loss in naïve CD4+ T cell priming, highlighting the critical link between diverse innate immune stimulation, NLRP10 activity and the immune function of mature DCs.
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3340615/
_version_ 1611526061325025280

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