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Series GSE243653 Query DataSets for GSE243653
Status Public on Jun 12, 2024
Title Single cell analysis uncovers striking cellular heterogeneity of lung infiltrating Tregs during steroid-responsive vs. steroid-resistant allergic airway inflammation
Organism Mus musculus
Experiment type Expression profiling by high throughput sequencing
Summary Allergic airway inflammation is a chronic inflammatory condition resulting from uncontrolled immune responses to environmental antigens. While it is well-established that allergic immune responses exhibit a high degree of diversity, driven by primary effector cell types like eosinophils, neutrophils, or CD4 T cells with distinct effector signatures, the exact mechanisms responsible for such pathogenesis remain largely elusive. Foxp3+ regulatory T cells (Treg) is an indispensable immune regulator during chronic inflammation including allergic airway inflammation. Emerging evidence suggests that Tregs infiltrating inflamed tissues exhibit distinct phenotypes dependent on the specific tissue sites and can display significant heterogeneity and tissue residency. Whether diverse allergic inflammatory responses in the lung influences infiltrating Treg heterogeneity or Treg lung residency has not previously been explored. We employed an unbiased single-cell RNAseq approach to study lung-infiltrating Tregs in models of eosinophilic and neutrophilic airway inflammation models, in which Tregs are critical immune regulators of inflammation. We found that lung-infiltrating Tregs are highly heterogeneous and that Tregs displaying lung residency phenotypes are significantly different depending on the types of inflammation. Tregs expression of ST2, a receptor for alarmin cytokine IL-33, was predominantly induced by eosinophilic inflammation and by tissue residency. However, Treg-specific ST2 deficiency did not affect the development of eosinophilic allergic inflammation nor the generation of lung resident Tregs. These results uncover a striking heterogeneity among Tregs infiltrating the lungs during allergic airway inflammation. The results also indicate that varying types of inflammation may give rise to phenotypically distinct lung resident Tregs. Thus, the present study underscores a novel mechanism by which inflammatory environments may shape the composition of infiltrating Tregs, allowing them to regulate inflammatory responses through tissue-adapted mechanisms.
Overall design The goal is to evaluate the cellular heterogeneity of Tregs that infiltrate the lung tissues during eosinophilic and neutrophilic airway inflammation. Experimental allergic airway inflammation was induced and lung infiltrating Tregs were FACS sorted for single cell analylsis.
Contributor(s) Iamsawat S, Yu R, Kim S, Liu K, Choi J
Citation(s) 38647384
Submission date Sep 20, 2023
Last update date Jun 13, 2024
Contact name Booki Min
Organization name Northwestern University
Department Microbiology-Immunology
Lab Booki Min
Street address 300 E. Superior Street
City Chicago
State/province IL
ZIP/Postal code 60611
Country USA
Platforms (1)
GPL24247 Illumina NovaSeq 6000 (Mus musculus)
Samples (2)
GSM7792345 Tregs, Aluminum, rep 1
GSM7792346 Tregs, CFA, rep 1
BioProject PRJNA1019336

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GSE243653_RAW.tar 128.7 Mb (http)(custom) TAR (of MTX, TSV)
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Raw data are available in SRA

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