ILC2-derived LIF licences progress from tissue to systemic immunity

Mayuri Gogoi (), Paula A. Clark, Ana C. F. Ferreira, Noe Rodriguez Rodriguez, Morgan Heycock, Michelle Ko, Jane E. Murphy, Victor Chen, Shi-Lu Luan, Helen E. Jolin and Andrew N. J. McKenzie ()
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Mayuri Gogoi: MRC Laboratory of Molecular Biology
Paula A. Clark: MRC Laboratory of Molecular Biology
Ana C. F. Ferreira: MRC Laboratory of Molecular Biology
Noe Rodriguez Rodriguez: MRC Laboratory of Molecular Biology
Morgan Heycock: MRC Laboratory of Molecular Biology
Michelle Ko: MRC Laboratory of Molecular Biology
Jane E. Murphy: MRC Laboratory of Molecular Biology
Victor Chen: MRC Laboratory of Molecular Biology
Shi-Lu Luan: MRC Laboratory of Molecular Biology
Helen E. Jolin: MRC Laboratory of Molecular Biology
Andrew N. J. McKenzie: MRC Laboratory of Molecular Biology

Nature, 2024, vol. 632, issue 8026, 885-892

Abstract: Abstract Migration and homing of immune cells are critical for immune surveillance. Trafficking is mediated by combinations of adhesion and chemokine receptors that guide immune cells, in response to chemokine signals, to specific locations within tissues and the lymphatic system to support tissue-localized immune reactions and systemic immunity1,2. Here we show that disruption of leukaemia inhibitory factor (LIF) production from group 2 innate lymphoid cells (ILC2s) prevents immune cells leaving the lungs to migrate to the lymph nodes (LNs). In the absence of LIF, viral infection leads to plasmacytoid dendritic cells (pDCs) becoming retained in the lungs where they improve tissue-localized, antiviral immunity, whereas chronic pulmonary allergen challenge leads to marked immune cell accumulation and the formation of tertiary lymphoid structures in the lung. In both cases immune cells fail to migrate to the lymphatics, leading to highly compromised LN reactions. Mechanistically, ILC2-derived LIF induces the production of the chemokine CCL21 from lymphatic endothelial cells lining the pulmonary lymphatic vessels, thus licensing the homing of CCR7+ immune cells (including dendritic cells) to LNs. Consequently, ILC2-derived LIF dictates the egress of immune cells from the lungs to regulate tissue-localized versus systemic immunity and the balance between allergen and viral responsiveness in the lungs.

Date: 2024
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DOI: 10.1038/s41586-024-07746-w

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