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Serum amyloid A is a soluble pattern recognition receptor that drives type 2 immunity
U. Smole, N. Gour, J. Phelan, G. Hofer, C. Köhler, B. Kratzer, PA. Tauber, X. Xiao, N. Yao, J. Dvorak, L. Caraballo, L. Puerta, S. Rosskopf, J. Chakir, E. Malle, AP. Lane, WF. Pickl, S. Lajoie, M. Wills-Karp,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
U19 AI070235
NIAID NIH HHS - United States
DC0190GP
CIHR - Canada
T32 ES007141
NIEHS NIH HHS - United States
R01 AI083315
NIAID NIH HHS - United States
R01 AI132590
NIAID NIH HHS - United States
R01 AI127644
NIAID NIH HHS - United States
R56 AI118791
NIAID NIH HHS - United States
NLK
ProQuest Central
od 2000-07-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 2000-07-01 do Před 1 rokem
Public Health Database (ProQuest)
od 2000-07-01 do Před 1 rokem
- MeSH
- alergeny imunologie MeSH
- alergická rýma imunologie patologie MeSH
- antigeny roztočů domácího prachu imunologie MeSH
- bronchiální astma imunologie patologie MeSH
- dospělí MeSH
- epitelové buňky MeSH
- humorální imunita MeSH
- interleukin 33 metabolismus MeSH
- kultivované buňky MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- mladý dospělý MeSH
- modely nemocí na zvířatech MeSH
- myši knockoutované MeSH
- myši MeSH
- plíce cytologie imunologie patologie MeSH
- primární buněčná kultura MeSH
- přirozená imunita MeSH
- proteiny vázající mastné kyseliny imunologie MeSH
- receptory lipoxinů metabolismus MeSH
- receptory pro formylované peptidy metabolismus MeSH
- respirační sliznice imunologie metabolismus MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- sérový amyloid A genetika metabolismus MeSH
- signální transdukce imunologie MeSH
- upregulace MeSH
- zvířata MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- myši MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
The molecular basis for the propensity of a small number of environmental proteins to provoke allergic responses is largely unknown. Herein, we report that mite group 13 allergens of the fatty acid-binding protein (FABP) family are sensed by an evolutionarily conserved acute-phase protein, serum amyloid A1 (SAA1), that promotes pulmonary type 2 immunity. Mechanistically, SAA1 interacted directly with allergenic mite FABPs (Der p 13 and Blo t 13). The interaction between mite FABPs and SAA1 activated the SAA1-binding receptor, formyl peptide receptor 2 (FPR2), which drove the epithelial release of the type-2-promoting cytokine interleukin (IL)-33 in a SAA1-dependent manner. Importantly, the SAA1-FPR2-IL-33 axis was upregulated in nasal epithelial cells from patients with chronic rhinosinusitis. These findings identify an unrecognized role for SAA1 as a soluble pattern recognition receptor for conserved FABPs found in common mite allergens that initiate type 2 immunity at mucosal surfaces.
Institute for Immunological Research University of Cartagena Cartagena Colombia
Institute of Molecular Biosciences BioTechMed Graz University of Graz Graz Austria
Citace poskytuje Crossref.org
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- $a Smole, Ursula $u Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. ursula.smole@irc.vib-ugent.be. Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria. ursula.smole@irc.vib-ugent.be.
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- $a Serum amyloid A is a soluble pattern recognition receptor that drives type 2 immunity / $c U. Smole, N. Gour, J. Phelan, G. Hofer, C. Köhler, B. Kratzer, PA. Tauber, X. Xiao, N. Yao, J. Dvorak, L. Caraballo, L. Puerta, S. Rosskopf, J. Chakir, E. Malle, AP. Lane, WF. Pickl, S. Lajoie, M. Wills-Karp,
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- $a The molecular basis for the propensity of a small number of environmental proteins to provoke allergic responses is largely unknown. Herein, we report that mite group 13 allergens of the fatty acid-binding protein (FABP) family are sensed by an evolutionarily conserved acute-phase protein, serum amyloid A1 (SAA1), that promotes pulmonary type 2 immunity. Mechanistically, SAA1 interacted directly with allergenic mite FABPs (Der p 13 and Blo t 13). The interaction between mite FABPs and SAA1 activated the SAA1-binding receptor, formyl peptide receptor 2 (FPR2), which drove the epithelial release of the type-2-promoting cytokine interleukin (IL)-33 in a SAA1-dependent manner. Importantly, the SAA1-FPR2-IL-33 axis was upregulated in nasal epithelial cells from patients with chronic rhinosinusitis. These findings identify an unrecognized role for SAA1 as a soluble pattern recognition receptor for conserved FABPs found in common mite allergens that initiate type 2 immunity at mucosal surfaces.
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