Evidence map›Paper›PMID 40503945›Full record

ArticleClinical and experimental immunology2025

Dendritic cell dysfunction, including impaired IL-12 production, is associated with chronic pulmonary aspergillosis.

Stefano A P Colombo, Sara Gago, Mathilde Chamula, Robert Lord, Andrew S MacDonald, Chris Kosmidis

Abstract read
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Article in Clinical and experimental immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Stefano A P ColomboLydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK.ORCID 0000-0002-3346-3437
Sara GagoManchester Fungal Infection Group, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
Mathilde ChamulaNational Aspergillosis Centre, Department of Infectious Diseases, Manchester University NHS Foundation Trust, Manchester, UK.
Robert LordLydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK.
Andrew S MacDonaldLydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK.
Chris KosmidisManchester Fungal Infection Group, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.ORCID 0000-0003-0662-1265

Funding

UK Research and Innovation - Newton Fund MR/S019898/1
6 · The paper itself

Abstract

backgroundGrowing evidence links immune dysfunction, notably impaired IFNγ production, to chronic pulmonary aspergillosis (CPA), but understanding of the immune phenotype in CPA patients remains limited.

methodsTo investigate this, we recruited 25 CPA patients and 25 controls with bronchiectasis, isolating immune cells from peripheral blood for detailed flow cytometric phenotyping at resting state and after ex vivo stimulation with the TLR2/Dectin-1 agonist Zymosan.

resultsCPA patients exhibited pronounced neutrophilia and a reduced frequency of conventional dendritic cell (DC) subsets at baseline compared to bronchiectasis controls. Post-stimulation, DC and monocyte subsets in CPA patients showed significantly lower expression of activation markers. Notably, cDC1s displayed reduced IL-12p40, TNFα, and CD86 expression. CPA patients with a history of tuberculosis (TB) had significantly higher frequencies of activated cDC1s. Machine learning analysis validated these immunological parameters as predictive of CPA status.

conclusionOur findings suggest that immune dysfunction in CPA involves DC and monocyte impairments, potentially contributing to IFNγ deficiency through reduced IL-12 production and co-stimulatory capacity in cDC1s. These results also hint at the presence of innate immune memory in CPA patients with prior TB. Our study advances understanding of the immune dysfunction underlying CPA.

Indexed as

Dendritic CellsInterleukin-12Pulmonary AspergillosisAdultAgedChronic DiseaseFemaleHumansInterferon-gammaMaleMiddle AgedMonocytesInterferon-gammaInterleukin-12cellular immunologycytokinesdendritic cellsfungal

Identifiers

PMID40503945
PMCPMC12231563

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.