Th1 responses in vivo require cell-specific provision of OX40L dictated by environmental cues

Dominika W. Gajdasik, Fabrina Gaspal, Emily E. Halford, Remi Fiancette, Emma E. Dutton, Claire Willis, Timo Rückert, Chiara Romagnani, Audrey Gerard, Sarah L. Bevington, Andrew S. MacDonald, Marina Botto, Timothy Vyse and David R. Withers ()
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Dominika W. Gajdasik: University of Birmingham
Fabrina Gaspal: University of Birmingham
Emily E. Halford: University of Birmingham
Remi Fiancette: University of Birmingham
Emma E. Dutton: University of Birmingham
Claire Willis: University of Birmingham
Timo Rückert: Charité - Universitätsmedizin Berlin
Chiara Romagnani: Charité - Universitätsmedizin Berlin
Audrey Gerard: The University of Oxford
Sarah L. Bevington: University of Birmingham
Andrew S. MacDonald: University of Manchester
Marina Botto: Imperial College London
Timothy Vyse: King’s College London
David R. Withers: University of Birmingham

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract The OX40-OX40L pathway provides crucial co-stimulatory signals for CD4 T cell responses, however the precise cellular interactions critical for OX40L provision in vivo and when these occur, remains unclear. Here, we demonstrate that provision of OX40L by dendritic cells (DCs), but not T cells, B cells nor group 3 innate lymphoid cells (ILC3s), is critical specifically for the effector Th1 response to an acute systemic infection with Listeria monocytogenes (Lm). OX40L expression by DCs is regulated by cross-talk with NK cells, with IFNγ signalling to the DC to enhance OX40L in a mechanism conserved in both mouse and human DCs. Strikingly, DC expression of OX40L is redundant in a chronic intestinal Th1 response and expression by ILC3s is necessary. Collectively these data reveal tissue specific compartmentalisation of the cellular provision of OX40L and define a mechanism controlling DC expression of OX40L in vivo.

Date: 2020
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DOI: 10.1038/s41467-020-17293-3

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