CD97/ADGRE5 attenuates the induction of adaptive type 2 immune responses in allergic asthma

Abstract Allergic asthma results from an uncontrolled type 2 immune response to inhaled allergens. Here, we investigate the function of CD97/ ADGRE5 , expressed in mouse and human immune and lung epithelial cells, in this disease. Female Cd97 −/− mice exhibit an exacerbated asthmatic phenotype across multiple models, primarily due to CD97 loss on immune cells. A single CD97 antibody treatment before allergen sensitization worsens allergic responses, highlighting a role for CD97 in early immune regulation. Post-sensitization, Cd97 −/− mice display higher frequencies of lung conventional type 2 and monocyte-derived dendritic cells (DCs). Allergen-pulsed Cd97 −/− bone marrow-derived DCs are more activated, promote enhanced proliferation and type 2 cytokine secretion by CD4⁺ OT-II cells, and induce stronger airway inflammation. Consistently, ADGRE5 expression is reduced in airway mucosa-derived mononuclear phagocyte subsets in human asthmatics after allergen-induced exacerbation. These results identify CD97 as an important regulator of DC-driven type 2 allergic responses and a potential target in asthma.

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Publication Details

Journal
Nature Communications
Published
2026-08-27
DOI
https://doi.org/10.1038/s41467-026-76948-9
Primary Topic
Receptor Mechanisms and Signaling
Type
article
Field-Weighted Citation Impact
0.00

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article

CD97/ADGRE5 attenuates the induction of adaptive type 2 immune responses in allergic asthma

Neal P. Smith, Marianne Quaas, Benjamin D. Medoff, Marita Wagner et al.
Nature Communications
Receptor Mechanisms and Signaling
article

CD97/ADGRE5 attenuates the induction of adaptive type 2 immune responses in allergic asthma

Neal P. Smith, Marianne Quaas, Benjamin D. Medoff, Marita Wagner, Christina Schofield, Knut Krohn, Anna-Lena Hoh, Tobias Polte, Alexandra–Chloé Villani, Ana Claudia Zenclussen, Jörg Hamann, Arkadiusz Pierzchalski, Christiane Kerner, Jehan Alladina, Gabriela Aust, Bingyu Wang, Matthias Steinert, Florian Höhna, Nele Häussler
article en

Abstract

Abstract Allergic asthma results from an uncontrolled type 2 immune response to inhaled allergens. Here, we investigate the function of CD97/ ADGRE5 , expressed in mouse and human immune and lung epithelial cells, in this disease. Female Cd97 −/− mice exhibit an exacerbated asthmatic phenotype across multiple models, primarily due to CD97 loss on immune cells. A single CD97 antibody treatment before allergen sensitization worsens allergic responses, highlighting a role for CD97 in early immune regulation. Post-sensitization, Cd97 −/− mice display higher frequencies of lung conventional type 2 and monocyte-derived dendritic cells (DCs). Allergen-pulsed Cd97 −/− bone marrow-derived DCs are more activated, promote enhanced proliferation and type 2 cytokine secretion by CD4⁺ OT-II cells, and induce stronger airway inflammation. Consistently, ADGRE5 expression is reduced in airway mucosa-derived mononuclear phagocyte subsets in human asthmatics after allergen-induced exacerbation. These results identify CD97 as an important regulator of DC-driven type 2 allergic responses and a potential target in asthma.

Nature CommunicationsVol. 17(1)
University of Iowa (US), Harvard University (US), Helmholtz Centre for Environmental Research (DE), Massachusetts General Hospital (US), University Hospital Leipzig (DE), Amsterdam University Medical Centers (NL), Martin Luther University Halle-Wittenberg (DE), University of Amsterdam (NL), Leipzig University (DE)
U.S. Department of Defense, Sanofi, Deutsche Forschungsgemeinschaft, National Institutes of Health
Good health and well-being
Openalex Percentile: Top 17%
Receptor Mechanisms and Signaling
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