Abstract | BACKGROUND: The earliest immune events induced by allergens are poorly understood, yet are likely essential to understanding how allergic inflammation is established. OBJECTIVE: We sought to describe the earliest signaling events activated by allergen and determine their significance to allergic inflammation. METHODS: RESULTS: CONCLUSION: FAP induces allergic lung inflammation through a previously unrecognized innate immune signaling mechanism. CLINICAL IMPLICATIONS: These findings reveal a new paradigm for understanding how allergic inflammation begins and suggest novel possibilities for the prevention and treatment of allergic diseases, such as asthma.
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Authors | Attila Kiss, Martin Montes, Sarat Susarla, Elin A Jaensson, Scott M Drouin, Rick A Wetsel, Zhengbin Yao, Rachel Martin, Nabeel Hamzeh, Rebecca Adelagun, Sheila Amar, Farrah Kheradmand, David B Corry |
Journal | The Journal of allergy and clinical immunology
(J Allergy Clin Immunol)
Vol. 120
Issue 2
Pg. 334-42
(Aug 2007)
ISSN: 0091-6749 [Print] United States |
PMID | 17544098
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Allergens
- Chemokines
- Fungal Proteins
- Receptors, Complement
- STAT6 Transcription Factor
- Toll-Like Receptor 4
- Interleukin-4
- Complement C3a
- Peptide Hydrolases
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Topics |
- Allergens
(immunology)
- Animals
- Aspergillus oryzae
(enzymology)
- Chemokines
(metabolism)
- Complement C3a
(metabolism)
- Eosinophils
(pathology)
- Fungal Proteins
(immunology)
- Gene Expression Regulation
- Hypersensitivity
(complications, genetics, immunology)
- Interleukin-4
(biosynthesis)
- Lung
(pathology)
- Mice
- Mice, Inbred Strains
- Peptide Hydrolases
(immunology, metabolism)
- Pneumonia
(etiology, pathology)
- Receptors, Complement
(metabolism)
- STAT6 Transcription Factor
(metabolism)
- Signal Transduction
- Th2 Cells
(pathology)
- Toll-Like Receptor 4
(metabolism)
- Transcription, Genetic
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