Antigen-presenting innate lymphoid cells orchestrate neuroinflammation.
John B Grigg1,2,3, Arthi Shanmugavadivu4, Tommy Regen4
1Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Nature
|December 2, 2021
Summary
Inflammatory group 3 innate lymphoid cells (ILC3s) promote T cell responses in the central nervous system (CNS), driving multiple sclerosis-like disease. Peripheral ILC3s may prevent this autoimmune neuroinflammation.
Area of Science:
- Neuroimmunology
- Immunology
- Cell Biology
Background:
- Pro-inflammatory T cells in the central nervous system (CNS) are linked to demyelinating and neurodegenerative diseases.
- The precise pathways controlling these T cell responses in the CNS are not fully understood.
Purpose of the Study:
- To define the role of innate lymphoid cells (ILCs) in the CNS during neuroinflammation.
- To investigate the function of group 3 innate lymphoid cells (ILC3s) in a mouse model of multiple sclerosis (MS).
Main Methods:
- Analysis of ILC3 populations in the CNS of a mouse model of MS.
- Assessment of ILC3 function as antigen-presenting cells (APCs) in the CNS.
- Investigation of ILC3s in human MS patients.
Main Results:
- A population of inflammatory ILC3s infiltrates the CNS, originates from circulation, and is found near T cells.
- These CNS ILC3s act as APCs, restimulating myelin-specific T cells and promoting disease.
- Elevated levels of these inflammatory ILC3s are observed in individuals with MS.
- Peripheral ILC3s, when targeted to present myelin antigen, limit autoimmune T cell responses and prevent disease.
Conclusions:
- Inflammatory ILC3s in the CNS are crucial drivers of T-cell-dependent neuroinflammation and MS-like disease.
- Peripheral tissue-resident ILC3s have a protective role and could be harnessed for autoimmune disease prevention.
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