Bet v 1 triggers antiviral-type immune signalling in birch-pollen-allergic individuals.


Journal

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
ISSN: 1365-2222
Titre abrégé: Clin Exp Allergy
Pays: England
ID NLM: 8906443

Informations de publication

Date de publication:
08 2022
Historique:
revised: 22 01 2022
received: 04 10 2021
accepted: 06 02 2022
pubmed: 12 2 2022
medline: 3 8 2022
entrez: 11 2 2022
Statut: ppublish

Résumé

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. To characterize the immune response to Bet v 1 in peripheral blood in patients allergic to birch pollen. 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. 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. 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.

Sections du résumé

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.

Identifiants

pubmed: 35147263
doi: 10.1111/cea.14108
pmc: PMC9540660
doi:

Substances chimiques

Allergens 0
Antigens, Plant 0
Antiviral Agents 0
Plant Proteins 0
Immunoglobulin E 37341-29-0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

929-941

Informations de copyright

© 2022 The Authors. Clinical & Experimental Allergy published by John Wiley & Sons Ltd.

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Auteurs

Lukas Wisgrill (L)

Division of Neonatology, Pediatric Intensive Care and Neuropediatrics, Comprehensive Center for Pediatrics, Medical University of Vienna, Vienna, Austria.
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Nanna Fyhrquist (N)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Human microbiome research program (HUMI), Medicum, University of Helsinki, Helsinki, Finland.

Joseph Ndika (J)

Human microbiome research program (HUMI), Medicum, University of Helsinki, Helsinki, Finland.

Laura Paalanen (L)

National Institute for Health and Welfare, Helsinki, Finland.
Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.

Angelika Berger (A)

Division of Neonatology, Pediatric Intensive Care and Neuropediatrics, Comprehensive Center for Pediatrics, Medical University of Vienna, Vienna, Austria.

Tiina Laatikainen (T)

National Institute for Health and Welfare, Helsinki, Finland.
Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.

Piia Karisola (P)

Human microbiome research program (HUMI), Medicum, University of Helsinki, Helsinki, Finland.

Tari Haahtela (T)

Skin and Allergy Hospital, Helsinki University Hospital, University of Helsinki, Helsinki, Finland.

Harri Alenius (H)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Human microbiome research program (HUMI), Medicum, University of Helsinki, Helsinki, Finland.

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