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Activation of group 2 innate lymphoid cells after allergen challenge in asthmatic patients

Winkler, Carla (author)
AstraZeneca, Sweden
Hochdoerfer, Thomas (author)
AstraZeneca, Sweden
Israelsson, Elisabeth (author)
AstraZeneca, Sweden
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Hasselberg, Annemarie (author)
AstraZeneca, Sweden
Cavallin, Anders (author)
AstraZeneca, Sweden
Thoern, Kristofer (author)
AstraZeneca, Sweden
Muthas, Daniel (author)
AstraZeneca, Sweden
Shojaee, Shervin (author)
AstraZeneca, Sweden
Lueer, Katrin (author)
Fraunhofer Inst Toxicol and Expt Med, Germany
Mueller, Meike (author)
Fraunhofer Inst Toxicol and Expt Med, Germany
Mjösberg, Jenny (author)
Karolinska Institutet,Linköpings universitet,Avdelningen för Kirurgi, Ortopedi och Onkologi,Medicinska fakulteten,Karolinska Inst, Sweden
Vaarala, Outi (author)
AstraZeneca, Sweden
Hohlfeld, Jens (author)
Fraunhofer Inst Toxicol and Expt Med, Germany; German Ctr Lung Res BREATH, Germany; Hannover Med Sch, Germany
Pardali, Katerina (author)
AstraZeneca, Sweden
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 (creator_code:org_t)
MOSBY-ELSEVIER, 2019
2019
English.
In: Journal of Allergy and Clinical Immunology. - : MOSBY-ELSEVIER. - 0091-6749 .- 1097-6825. ; 144:1, s. 61-
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Background: Group 2 innate lymphoid cells (ILC2s) are effective producers of IL-5 and IL-13 during allergic inflammation and bridge the innate and adaptive immune responses. ILC2 numbers are increased in asthmatic patients compared with healthy control subjects. Thus far, human data describing their phenotype during acute allergic inflammation in the lung are incomplete. Objectives: This study aims to characterize and compare blood and lung-derived ILC2s before and after segmental allergen challenge in patients with mild-to-moderate asthma with high blood eosinophil counts (amp;gt;= 300 cells/mu L). Methods: ILC2s were isolated from blood and bronchoalveolar lavage (BAL) fluid before and after segmental allergen challenge. Cells were sorted by means of flow cytometry, cultured and analyzed for cytokine release or migration, and sequenced for RNA expression. Results: ILC2s were nearly absent in the alveolar space under baseline conditions, but numbers increased significantly after allergen challenge (P amp;lt; .05), whereas at the same time, ILC2 numbers in blood were reduced (P amp;lt; .05). Prostaglandin D2 and CXCL12 levels in BAL fluid correlated with decreased ILC2 numbers in blood (P = .004, respective P = .024). After allergen challenge, several genes promoting type 2 inflammation were expressed at greater levels in BAL fluid compared with blood ILC2s, whereas blood ILC2s remain unactivated. Conclusion: ILC2s accumulate at the site of allergic inflammation and are recruited from the blood. Their transcriptional and functional activation pattern promotes type 2 inflammation.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Lungmedicin och allergi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Respiratory Medicine and Allergy (hsv//eng)

Keyword

Group 2 innate lymphoid cells; allergic asthma; allergen challenge; migration; gene expression

Publication and Content Type

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