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Transcriptional signature of human pro-inflammatory T(H)17 cells identifies reduced IL10 gene expression in multiple sclerosis

Journal article
Authors D. Hu
S. Notarbartolo
T. Croonenborghs
B. Patel
R. Cialic
T. H. Yang
D. Aschenbrenner
Karin Andersson
M. Gattorno
M. Pham
P. Kivisakk
I. V. Pierre
Y. Lee
K. Kiani
Maria Bokarewa
E. Tjon
N. Pochet
F. Sallusto
V. K. Kuchroo
H. L. Weiner
Published in Nature Communications
Volume 8
Issue 1
ISSN 2041-1723
Publication year 2017
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Language en
Keywords experimental autoimmune encephalomyelitis, set enrichment analysis, central-nervous-system, hyper-ige syndrome, th17 cells, ifn-gamma, t-cells, disease, bet, induction, Science & Technology - Other Topics
Subject categories Rheumatology and Autoimmunity


We have previously reported the molecular signature of murine pathogenic T(H)17 cells that induce experimental autoimmune encephalomyelitis (EAE) in animals. Here we show that human peripheral blood IFN-gamma(+) IL-17(+) (T(H)1/17) and IFN-gamma(-)-IL-17(+) (T(H)17) CD4(+) T cells display distinct transcriptional profiles in high-throughput transcription analyses. Compared to T(H)17 cells, T(H)1/17 cells have gene signatures with marked similarity to mouse pathogenic T(H)17 cells. Assessing 15 representative signature genes in patients with multiple sclerosis, we find that T(H)1/17 cells have elevated expression of CXCR3 and reduced expression of IFNG, CCL3, CLL4, GZMB, and IL10 compared to healthy controls. Moreover, higher expression of IL10 in T(H)17 cells is found in clinically stable vs. active patients. Our results define the molecular signature of human pro-inflammatory T(H)17 cells, which can be used to both identify pathogenic T(H)17 cells and to measure the effect of treatment on T(H)17 cells in human autoimmune diseases.

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