High-dimensional profiling reveals Tc17 cell enrichment in active Crohn’s disease and identifies a potentially targetable signature

A.-M. Globig, A. V. Hipp, P. Otto-Mora, M. Heeg, L. S. Mayer, S. Ehl, H. Schwacha, M. Bewtra, V. Tomov, R. Thimme, P. Hasselblatt and B. Bengsch ()
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A.-M. Globig: Faculty of Medicine, University Medical Center Freiburg
A. V. Hipp: Faculty of Medicine, University Medical Center Freiburg
P. Otto-Mora: Faculty of Medicine, University Medical Center Freiburg
M. Heeg: Faculty of Medicine, University Medical Center Freiburg
L. S. Mayer: Faculty of Medicine, University Medical Center Freiburg
S. Ehl: Faculty of Medicine, University Medical Center Freiburg
H. Schwacha: Faculty of Medicine, University Medical Center Freiburg
M. Bewtra: University of Pennsylvania Perelman School of Medicine
V. Tomov: University of Pennsylvania Perelman School of Medicine
R. Thimme: Faculty of Medicine, University Medical Center Freiburg
P. Hasselblatt: Faculty of Medicine, University Medical Center Freiburg
B. Bengsch: Faculty of Medicine, University Medical Center Freiburg

Nature Communications, 2022, vol. 13, issue 1, 1-15

Abstract: Abstract The immune-pathology in Crohn’s disease is linked to dysregulated CD4+ T cell responses biased towards pathogenic TH17 cells. However, the role of CD8+ T cells able to produce IL-17 (Tc17 cells) remains unclear. Here we characterize the peripheral blood and intestinal tissue of Crohn’s disease patients (n = 61) with flow and mass cytometry and reveal a strong increase of Tc17 cells in active disease, mainly due to induction of conventional T cells. Mass cytometry shows that Tc17 cells express a distinct immune signature (CD6high, CD39, CD69, PD-1, CD27low) which was validated in an independent patient cohort. This signature stratifies patients into groups with distinct flare-free survival associated with differential CD6 expression. Targeting of CD6 in vitro reduces IL-17, IFN-γ and TNF production. These results identify a distinct Tc17 cell population in Crohn’s disease with proinflammatory features linked to disease activity. The Tc17 signature informs clinical outcomes and may guide personalized treatment decisions.

Date: 2022
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DOI: 10.1038/s41467-022-31229-z

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