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Publication : Dynamic trafficking patterns of IL-17-producing γδ T cells are linked to the recurrence of skin inflammation in psoriasis-like dermatitis.

First Author  Liu N Year  2022
Journal  EBioMedicine Volume  82
Pages  104136 PubMed ID  35785620
Mgi Jnum  J:351500 Mgi Id  MGI:7310574
Doi  10.1016/j.ebiom.2022.104136 Citation  Liu N, et al. (2022) Dynamic trafficking patterns of IL-17-producing gammadelta T cells are linked to the recurrence of skin inflammation in psoriasis-like dermatitis. EBioMedicine 82:104136
abstractText  BACKGROUND: Psoriasis recurrence is a clinically challenging issue. However, the underlying mechanisms haven't been fully understood. METHODS: RNAseq analysis from affected skin of psoriatic patients treated with topical glucocorticoid (GC) with different outcomes was performed. In addition, imiquimod (IMQ)-induced mouse psoriasis-like model was used to mimic GC treatment in human psoriasis patients. Skin tissues and draining and distant lymph nodes (LNs) were harvested for flow cytometry and histology analyses. FINDINGS: RNAseq analysis revealed that chemokine and chemokine receptor gene expression was decreased in post-treated skin compared to pre-treated samples but was subsequently increased in the recurred skin. In IMQ-induced mouse psoriasis-like model, we found that gammadeltaT17 cells were decreased in the skin upon topical GC treatment but surprisingly increased in the draining and distant LNs. This redistribution pattern lasted even two weeks post GC withdrawal. Upon IMQ re-challenge on the same site, mice previously treated with GC developed more severe skin inflammation. There were gammadeltaT17 cells migrated from LNs to the skin. This dynamic trafficking was dependent on CCR6 as this phenomenon was completely abrogated in CCR6-deficient mice. In addition, inhibition of lymphocyte egress prevented this heightened skin inflammation induced by IMQ rechallenge. INTERPRETATION: Redistribution of pathogenic gammadeltaT17 cells may be vital to prevent disease recurrence and this model of psoriasis-like dermatitis. FUNDING: This work was supported by National Natural Science Foundation of China 81830095/H1103, 81761128008/H10 (J.Z.) and the NIH R01AI128818 and the National Psoriasis Foundation (J.Y.).
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