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Bet v 1 triggers antiviral‐type immune signalling in birch‐pollen‐allergic individuals
BACKGROUND: In allergic patients, clinical symptoms caused by pollen remind of symptoms triggered by viral respiratory infections, which are also the main cause of asthmatic exacerbations. In patients sensitized to birch pollen, Bet v 1 is the major symptom‐causing allergen. Immune mechanisms drivin...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9540660/ https://www.ncbi.nlm.nih.gov/pubmed/35147263 http://dx.doi.org/10.1111/cea.14108 |
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author | Wisgrill, Lukas Fyhrquist, Nanna Ndika, Joseph Paalanen, Laura Berger, Angelika Laatikainen, Tiina Karisola, Piia Haahtela, Tari Alenius, Harri |
author_facet | Wisgrill, Lukas Fyhrquist, Nanna Ndika, Joseph Paalanen, Laura Berger, Angelika Laatikainen, Tiina Karisola, Piia Haahtela, Tari Alenius, Harri |
author_sort | Wisgrill, Lukas |
collection | PubMed |
description | BACKGROUND: In allergic patients, clinical symptoms caused by pollen remind of symptoms triggered by viral respiratory infections, which are also the main cause of asthmatic exacerbations. In patients sensitized to birch pollen, Bet v 1 is the major symptom‐causing allergen. Immune mechanisms driving Bet v 1‐related responses of human blood cells have not been fully characterized. OBJECTIVE: To characterize the immune response to Bet v 1 in peripheral blood in patients allergic to birch pollen. METHODS: The peripheral blood mononuclear cells of birch‐allergic (n = 24) and non‐allergic (n = 47) adolescents were stimulated ex‐vivo followed by transcriptomic profiling. Systems‐biology approaches were employed to decipher disease‐relevant gene networks and deconvolution of associated cell populations. RESULTS: Solely in birch‐allergic patients, co‐expression analysis revealed activation of networks of innate immunity and antiviral signalling as the immediate response to Bet v 1 stimulation. Toll‐like receptors and signal transducer transcription were the main drivers of gene expression patterns. Macrophages and dendritic cells were the main cell subsets responding to Bet v 1. CONCLUSIONS AND CLINICAL RELEVANCE: In birch‐pollen‐allergic patients, the activated innate immune networks seem to be, in part, the same as those activated during viral infections. This tendency of the immune system to read pollens as viruses may provide new insight to allergy prevention and treatment. |
format | Online Article Text |
id | pubmed-9540660 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-95406602022-10-14 Bet v 1 triggers antiviral‐type immune signalling in birch‐pollen‐allergic individuals Wisgrill, Lukas Fyhrquist, Nanna Ndika, Joseph Paalanen, Laura Berger, Angelika Laatikainen, Tiina Karisola, Piia Haahtela, Tari Alenius, Harri Clin Exp Allergy Original Articles BACKGROUND: In allergic patients, clinical symptoms caused by pollen remind of symptoms triggered by viral respiratory infections, which are also the main cause of asthmatic exacerbations. In patients sensitized to birch pollen, Bet v 1 is the major symptom‐causing allergen. Immune mechanisms driving Bet v 1‐related responses of human blood cells have not been fully characterized. OBJECTIVE: To characterize the immune response to Bet v 1 in peripheral blood in patients allergic to birch pollen. METHODS: The peripheral blood mononuclear cells of birch‐allergic (n = 24) and non‐allergic (n = 47) adolescents were stimulated ex‐vivo followed by transcriptomic profiling. Systems‐biology approaches were employed to decipher disease‐relevant gene networks and deconvolution of associated cell populations. RESULTS: Solely in birch‐allergic patients, co‐expression analysis revealed activation of networks of innate immunity and antiviral signalling as the immediate response to Bet v 1 stimulation. Toll‐like receptors and signal transducer transcription were the main drivers of gene expression patterns. Macrophages and dendritic cells were the main cell subsets responding to Bet v 1. CONCLUSIONS AND CLINICAL RELEVANCE: In birch‐pollen‐allergic patients, the activated innate immune networks seem to be, in part, the same as those activated during viral infections. This tendency of the immune system to read pollens as viruses may provide new insight to allergy prevention and treatment. John Wiley and Sons Inc. 2022-02-18 2022-08 /pmc/articles/PMC9540660/ /pubmed/35147263 http://dx.doi.org/10.1111/cea.14108 Text en © 2022 The Authors. Clinical & Experimental Allergy published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Original Articles Wisgrill, Lukas Fyhrquist, Nanna Ndika, Joseph Paalanen, Laura Berger, Angelika Laatikainen, Tiina Karisola, Piia Haahtela, Tari Alenius, Harri Bet v 1 triggers antiviral‐type immune signalling in birch‐pollen‐allergic individuals |
title | Bet v 1 triggers antiviral‐type immune signalling in birch‐pollen‐allergic individuals |
title_full | Bet v 1 triggers antiviral‐type immune signalling in birch‐pollen‐allergic individuals |
title_fullStr | Bet v 1 triggers antiviral‐type immune signalling in birch‐pollen‐allergic individuals |
title_full_unstemmed | Bet v 1 triggers antiviral‐type immune signalling in birch‐pollen‐allergic individuals |
title_short | Bet v 1 triggers antiviral‐type immune signalling in birch‐pollen‐allergic individuals |
title_sort | bet v 1 triggers antiviral‐type immune signalling in birch‐pollen‐allergic individuals |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9540660/ https://www.ncbi.nlm.nih.gov/pubmed/35147263 http://dx.doi.org/10.1111/cea.14108 |
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