Unique transcriptome signatures and GM-CSF expression in lymphocytes from patients with spondyloarthritis

M. H. Al-Mossawi (), L. Chen, H. Fang, A. Ridley, J. Wit, N. Yager, A. Hammitzsch, I. Pulyakhina, B. P. Fairfax, D. Simone, Yao Yi, S. Bandyopadhyay, K. Doig, R Gundle, B. Kendrick, F. Powrie, J. C. Knight and P. Bowness
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M. H. Al-Mossawi: University of Oxford
L. Chen: University of Oxford
H. Fang: University of Oxford
A. Ridley: University of Oxford
J. Wit: University of Oxford
N. Yager: University of Oxford
A. Hammitzsch: University of Oxford
I. Pulyakhina: University of Oxford
B. P. Fairfax: University of Oxford
D. Simone: University of Oxford
Yao Yi: University of Oxford
S. Bandyopadhyay: University of Oxford
K. Doig: University of Oxford
R Gundle: University of Oxford
B. Kendrick: University of Oxford
F. Powrie: University of Oxford
J. C. Knight: University of Oxford
P. Bowness: University of Oxford

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Spondyloarthritis encompasses a group of common inflammatory diseases thought to be driven by IL-17A-secreting type-17 lymphocytes. Here we show increased numbers of GM-CSF-producing CD4 and CD8 lymphocytes in the blood and joints of patients with spondyloarthritis, and increased numbers of IL-17A+GM-CSF+ double-producing CD4, CD8, γδ and NK cells. GM-CSF production in CD4 T cells occurs both independently and in combination with classical Th1 and Th17 cytokines. Type 3 innate lymphoid cells producing predominantly GM-CSF are expanded in synovial tissues from patients with spondyloarthritis. GM-CSF+CD4+ cells, isolated using a triple cytokine capture approach, have a specific transcriptional signature. Both GM-CSF+ and IL-17A+GM-CSF+ double-producing CD4 T cells express increased levels of GPR65, a proton-sensing receptor associated with spondyloarthritis in genome-wide association studies and pathogenicity in murine inflammatory disease models. Silencing GPR65 in primary CD4 T cells reduces GM-CSF production. GM-CSF and GPR65 may thus serve as targets for therapeutic intervention of spondyloarthritis.

Date: 2017
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DOI: 10.1038/s41467-017-01771-2

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