| Autor: |
Koen Venken, Jacques, Peggy, Mortier, Céline, Labadia, Mark E., Decruy, Tine, Coudenys, Julie, Hoyt, Kathleen, Wayne, Anita L., Hughes, Robert, Turner, Michael, Van Gassen, Sofie, Martens, Liesbet, Smith, Dustin, Harcken, Christian, Wahle, Joseph, Chao-Ting Wang, Verheugen, Eveline, Schryvers, Nadia, Varkas, Gaëlle, Cypers, Heleen |
| Zdroj: |
Nature Communications; 1/2/2019, Vol. 10 Issue 1, p1-15, 15p, 6 Graphs |
| Abstrakt: |
Dysregulated IL-23/IL-17 responses have been linked to psoriatic arthritis and other forms of spondyloarthritides (SpA). RORγt, the key Thelper17 (Th17) cell transcriptional regulator, is also expressed by subsets of innate-like T cells, including invariant natural killer T (iNKT) and γδ-T cells, but their contribution to SpA is still unclear. Here we describe the presence of particular RORγt+T-betloPLZF--iNKT and γδ-hi T cell subsets in healthy peripheral blood. RORγt+ iNKT and γδ-hi T cells show IL-23 mediated Th17-like immune responses and were clearly enriched within inflamed joints of SpA patients where they act as major IL-17 secretors. SpA derived iNKT and γδ-T cells showed unique and Th17-skewed phenotype and gene expression profiles. Strikingly, RORγt inhibition blocked γδ17 and iNKT17 cell function while selectively sparing IL-22+ subsets. Overall, our findings highlight a unique diversity of human RORγt+ T cells and underscore the potential of RORγt antagonism to modulate aberrant type 17 responses. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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