The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.
Adventitial Stromal Cells Define Group 2 Innate Lymphoid Cell Tissue Niches
Open accessAbstract
&NA; Type 2 lymphocytes promote both physiologic tissue remodeling and allergic pathology, yet their physical tissue niches are poorly described. Here, we used quantitative imaging to define the tissue niches of group 2 innate lymphoid cells (ILC2s), which are critical instigators of type 2 immunity. We identified a dominant adventitial niche around lung bronchi and larger vessels in multiple tissues, where ILC2s localized with subsets of dendritic and regulatory T cells. However, ILC2s were most intimately associated with adventitial stromal cells (ASCs), a mesenchymal fibroblast‐like subset that expresses interleukin‐33 (IL‐33) and thymic stromal lymphopoietin (TSLP). In vitro, ASCs produced TSLP that supported ILC2 accumulation and activation. ILC2s and IL‐13 drove reciprocal ASC expansion and IL‐33 expression. During helminth infection, ASC depletion impaired lung ILC2 and Th2 cell accumulation and function, which are in part dependent on ASC‐derived IL‐33. These data indicate that adventitial niches are conserved sites where ASCs regulate type 2 lymphocyte expansion and function. Graphical Abstract Figure. No caption available. Highlights3D imaging defines ILC2 niches in perivascular regions of multiple tissuesILC2s localize with fibroblast‐like adventitial stromal cells (ASCs)Lung ASCs produce IL‐33 and TSLP to support ILC2 and Th2sILC2s promote ASC expansion and IL‐33 production after helminth infection
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Cites
Spatial reconstruction of single-cell gene expression data
Satija, R., Farrell, J. A., Gennert, D., Schier, A. F., & Regev, A. (2015) · Nature Biotechnology · doi:10.1038/nbt.3192 · Cited by 7,055
Innate Lymphoid Cells: 10 Years On
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A gene expression atlas of the central nervous system based on bacterial artificial chromosomes
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Mapping the Mouse Cell Atlas by Microwell-Seq
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Type 2 innate lymphoid cells control eosinophil homeostasis
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Self-citationInnate lymphoid cells as regulators of immunity, inflammation and tissue homeostasis
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Perivascular Gli1+ Progenitors Are Key Contributors to Injury-Induced Organ Fibrosis
Kramann, R., Schneider, R. K., DiRocco, D. P., Machado, F., Fleig, S., Bondzie, P. A., Henderson, J. M., Ebert, B. L., & Humphreys, B. D. (2015) · Cell Stem Cell · doi:10.1016/j.stem.2014.11.004 · Cited by 922 · cited 4×
“We confirmed that ASCs co-expressed Gli1, Sca1, and Gp38 in bronchovascular cuffs and several other perivascular regions (Kramann et al., 2015), accounting for over 80% of total lung Gli1 cells at rest and after type 2 stimuli (Figures 7A, 7D, and S7A–S7D).”
InfluentialInterleukin‐33 (IL‐33): A nuclear cytokine from the IL‐1 family
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In Vivo CD4 + T Cell Differentiation and Function: Revisiting the Th1/Th2 Paradigm
Ruterbusch, M., Pruner, K. B., Shehata, L., & Pepper, M. (2020) · Annual Review of Immunology · doi:10.1146/annurev-immunol-103019-085803 · Cited by 550
He, H., Suryawanshi, H., Morozov, P., Gay-Mimbrera, J., Del Duca, E., Kim, H. J., Kameyama, N., Estrada, Y., Der, E., Krueger, J. G., et al. (2020) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2020.01.042 · Cited by 503
Metadata
- Authors
- Dahlgren, M. W., Jones, S. W., Cautivo, K. M., Dubinin, A., Ortiz-Carpena, J. F., Farhat, S., Yu, K. S., Lee, K., Wang, C., Molofsky, A. V., Tward, A. D., Krummel, M. F., Peng, T., & Molofsky, A. B.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2019-03
- Volume
- 50
- Issue
- 3
- Pages
- 707-722.e6
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2915312760
- Cited by
- 353
- References
- 53
- FWCI
- 13.70
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Dahlgren, M. W., Jones, S. W., Cautivo, K. M., Dubinin, A., Ortiz-Carpena, J. F., Farhat, S., Yu, K. S., Lee, K., Wang, C., Molofsky, A. V., Tward, A. D., Krummel, M. F., Peng, T., & Molofsky, A. B. (2019). Adventitial Stromal Cells Define Group 2 Innate Lymphoid Cell Tissue Niches. Immunity. https://doi.org/10.1016/j.immuni.2019.02.002
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