ILC3s control splenic cDC homeostasis via lymphotoxin signaling
- Author
- Matthias Vanderkerken, Antonio Pires da Silva Baptista (UGent) , Marco De Giovanni, Satoshi Fukuyama, Robin Browaeys (UGent) , Charlotte Scott (UGent) , Paula S. Norris, Gerard Eberl, James P. Di Santo, Eric Vivier, Yvan Saeys (UGent) , Hamida Hammad (UGent) , Jason G. Cyster, Carl F. Ware, Alexei V. Tumanov, Carl De Trez and Bart Lambrecht (UGent)
- Organization
- Abstract
- The spleen contains a myriad of conventional dendritic cell (cDC) subsets that protect against systemic pathogen dissemination by bridging antigen detection to the induction of adaptive immunity. How cDC subsets differentiate in the splenic environment is poorly understood. Here, we report that LTα1β2-expressing Rorgt+ ILC3s, together with B cells, control the splenic cDC niche size and the terminal differentiation of Sirpα+CD4+Esam+ cDC2s, independently of the microbiota and of bone marrow pre-cDC output. Whereas the size of the splenic cDC niche depended on lymphotoxin signaling only during a restricted time frame, the homeostasis of Sirpα+CD4+Esam+ cDC2s required continuous lymphotoxin input. This latter property made Sirpα+CD4+Esam+ cDC2s uniquely susceptible to pharmacological interventions with LTβR agonists and antagonists and to ILC reconstitution strategies. Together, our findings demonstrate that LTα1β2-expressing Rorgt+ ILC3s drive splenic cDC differentiation and highlight the critical role of ILC3s as perpetual regulators of lymphoid tissue homeostasis.
- Keywords
- Immunology, Immunology and Allergy, INNATE LYMPHOID-CELLS, SUBCAPSULAR SINUS MACROPHAGES, CONVENTIONAL DENDRITIC CELLS, BETA-RECEPTOR, R PACKAGE, B-CELLS, IN-VITRO, SUBSETS, ZONE, EXPRESSION
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-8707612
- MLA
- Vanderkerken, Matthias, et al. “ILC3s Control Splenic CDC Homeostasis via Lymphotoxin Signaling.” JOURNAL OF EXPERIMENTAL MEDICINE, vol. 218, no. 5, 2021, doi:10.1084/jem.20190835.
- APA
- Vanderkerken, M., Pires da Silva Baptista, A., De Giovanni, M., Fukuyama, S., Browaeys, R., Scott, C., … Lambrecht, B. (2021). ILC3s control splenic cDC homeostasis via lymphotoxin signaling. JOURNAL OF EXPERIMENTAL MEDICINE, 218(5). https://doi.org/10.1084/jem.20190835
- Chicago author-date
- Vanderkerken, Matthias, Antonio Pires da Silva Baptista, Marco De Giovanni, Satoshi Fukuyama, Robin Browaeys, Charlotte Scott, Paula S. Norris, et al. 2021. “ILC3s Control Splenic CDC Homeostasis via Lymphotoxin Signaling.” JOURNAL OF EXPERIMENTAL MEDICINE 218 (5). https://doi.org/10.1084/jem.20190835.
- Chicago author-date (all authors)
- Vanderkerken, Matthias, Antonio Pires da Silva Baptista, Marco De Giovanni, Satoshi Fukuyama, Robin Browaeys, Charlotte Scott, Paula S. Norris, Gerard Eberl, James P. Di Santo, Eric Vivier, Yvan Saeys, Hamida Hammad, Jason G. Cyster, Carl F. Ware, Alexei V. Tumanov, Carl De Trez, and Bart Lambrecht. 2021. “ILC3s Control Splenic CDC Homeostasis via Lymphotoxin Signaling.” JOURNAL OF EXPERIMENTAL MEDICINE 218 (5). doi:10.1084/jem.20190835.
- Vancouver
- 1.Vanderkerken M, Pires da Silva Baptista A, De Giovanni M, Fukuyama S, Browaeys R, Scott C, et al. ILC3s control splenic cDC homeostasis via lymphotoxin signaling. JOURNAL OF EXPERIMENTAL MEDICINE. 2021;218(5).
- IEEE
- [1]M. Vanderkerken et al., “ILC3s control splenic cDC homeostasis via lymphotoxin signaling,” JOURNAL OF EXPERIMENTAL MEDICINE, vol. 218, no. 5, 2021.
@article{8707612,
abstract = {{The spleen contains a myriad of conventional dendritic cell (cDC) subsets that protect against systemic pathogen dissemination by bridging antigen detection to the induction of adaptive immunity. How cDC subsets differentiate in the splenic environment is poorly understood. Here, we report that LTα1β2-expressing Rorgt+ ILC3s, together with B cells, control the splenic cDC niche size and the terminal differentiation of Sirpα+CD4+Esam+ cDC2s, independently of the microbiota and of bone marrow pre-cDC output. Whereas the size of the splenic cDC niche depended on lymphotoxin signaling only during a restricted time frame, the homeostasis of Sirpα+CD4+Esam+ cDC2s required continuous lymphotoxin input. This latter property made Sirpα+CD4+Esam+ cDC2s uniquely susceptible to pharmacological interventions with LTβR agonists and antagonists and to ILC reconstitution strategies. Together, our findings demonstrate that LTα1β2-expressing Rorgt+ ILC3s drive splenic cDC differentiation and highlight the critical role of ILC3s as perpetual regulators of lymphoid tissue homeostasis.}},
articleno = {{e20190835}},
author = {{Vanderkerken, Matthias and Pires da Silva Baptista, Antonio and De Giovanni, Marco and Fukuyama, Satoshi and Browaeys, Robin and Scott, Charlotte and Norris, Paula S. and Eberl, Gerard and Di Santo, James P. and Vivier, Eric and Saeys, Yvan and Hammad, Hamida and Cyster, Jason G. and Ware, Carl F. and Tumanov, Alexei V. and De Trez, Carl and Lambrecht, Bart}},
issn = {{0022-1007}},
journal = {{JOURNAL OF EXPERIMENTAL MEDICINE}},
keywords = {{Immunology,Immunology and Allergy,INNATE LYMPHOID-CELLS,SUBCAPSULAR SINUS MACROPHAGES,CONVENTIONAL DENDRITIC CELLS,BETA-RECEPTOR,R PACKAGE,B-CELLS,IN-VITRO,SUBSETS,ZONE,EXPRESSION}},
language = {{eng}},
number = {{5}},
pages = {{20}},
title = {{ILC3s control splenic cDC homeostasis via lymphotoxin signaling}},
url = {{http://doi.org/10.1084/jem.20190835}},
volume = {{218}},
year = {{2021}},
}
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