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© Research
Publication : The Journal of experimental medicine

ILC3s control splenic cDC homeostasis via lymphotoxin signaling.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of experimental medicine - 03 May 2021

Vanderkerken M, Baptista AP, De Giovanni M, Fukuyama S, Browaeys R, Scott CL, Norris PS, Eberl G, Di Santo JP, Vivier E, Saeys Y, Hammad H, Cyster JG, Ware CF, Tumanov AV, De Trez C, Lambrecht BN,

Link to Pubmed [PMID] – 33724364

Link to DOI – e2019083510.1084/jem.20190835

J Exp Med 2021 May; 218(5):

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.

https://pubmed.ncbi.nlm.nih.gov/33724364