Antigen-presenting innate lymphoid cells orchestrate neuroinflammation

John B. Grigg, Arthi Shanmugavadivu, Tommy Regen, Christopher N. Parkhurst, Anees Ahmed, Ann M. Joseph, Michael Mazzucco, Konrad Gronke, Andreas Diefenbach, Gerard Eberl, Timothy Vartanian, Ari Waisman and Gregory F. Sonnenberg ()
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John B. Grigg: Cornell University
Arthi Shanmugavadivu: University Medical Center of the Johannes Gutenberg University Mainz
Tommy Regen: University Medical Center of the Johannes Gutenberg University Mainz
Christopher N. Parkhurst: Cornell University
Anees Ahmed: Cornell University
Ann M. Joseph: Cornell University
Michael Mazzucco: Cornell University
Konrad Gronke: Charité—Universitätsmedizin Berlin
Andreas Diefenbach: Charité—Universitätsmedizin Berlin
Gerard Eberl: Institut Pasteur
Timothy Vartanian: Cornell University
Ari Waisman: University Medical Center of the Johannes Gutenberg University Mainz
Gregory F. Sonnenberg: Cornell University

Nature, 2021, vol. 600, issue 7890, 707-712

Abstract: Abstract Pro-inflammatory T cells in the central nervous system (CNS) are causally associated with multiple demyelinating and neurodegenerative diseases1–6, but the pathways that control these responses remain unclear. Here we define a population of inflammatory group 3 innate lymphoid cells (ILC3s) that infiltrate the CNS in a mouse model of multiple sclerosis. These ILC3s are derived from the circulation, localize in proximity to infiltrating T cells in the CNS, function as antigen-presenting cells that restimulate myelin-specific T cells, and are increased in individuals with multiple sclerosis. Notably, antigen presentation by inflammatory ILC3s is required to promote T cell responses in the CNS and the development of multiple-sclerosis-like disease in mouse models. By contrast, conventional and tissue-resident ILC3s in the periphery do not appear to contribute to disease induction, but instead limit autoimmune T cell responses and prevent multiple-sclerosis-like disease when experimentally targeted to present myelin antigen. Collectively, our data define a population of inflammatory ILC3s that is essential for directly promoting T-cell-dependent neuroinflammation in the CNS and reveal the potential of harnessing peripheral tissue-resident ILC3s for the prevention of autoimmune disease.

Date: 2021
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DOI: 10.1038/s41586-021-04136-4

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