Version 1
: Received: 2 September 2024 / Approved: 2 September 2024 / Online: 2 September 2024 (09:57:19 CEST)
How to cite:
Kim, H.; Zheng, M.; Ahn, S.; Park, I. G.; Noh, M.; Sung, J.-H. Involvement of RIPK1 in Alopecia Areata. Preprints2024, 2024090082. https://doi.org/10.20944/preprints202409.0082.v1
Kim, H.; Zheng, M.; Ahn, S.; Park, I. G.; Noh, M.; Sung, J.-H. Involvement of RIPK1 in Alopecia Areata. Preprints 2024, 2024090082. https://doi.org/10.20944/preprints202409.0082.v1
Kim, H.; Zheng, M.; Ahn, S.; Park, I. G.; Noh, M.; Sung, J.-H. Involvement of RIPK1 in Alopecia Areata. Preprints2024, 2024090082. https://doi.org/10.20944/preprints202409.0082.v1
APA Style
Kim, H., Zheng, M., Ahn, S., Park, I. G., Noh, M., & Sung, J. H. (2024). Involvement of RIPK1 in Alopecia Areata. Preprints. https://doi.org/10.20944/preprints202409.0082.v1
Chicago/Turabian Style
Kim, H., Minsoo Noh and Jong-Hyuk Sung. 2024 "Involvement of RIPK1 in Alopecia Areata" Preprints. https://doi.org/10.20944/preprints202409.0082.v1
Abstract
We have previously demonstrated that receptor-interacting serine threonine kinase 1 (RIPK1) is expressed in hair follicle and regulates hair cycle. RIPK1 inhibitors also accelerated the telogen-to-anagen transition and elongated the anagen period in the mouse model. Here, we first investigated the involvement of RIPK1 in alopecia areata (AA). mRNA and protein expression of RIPK1 was increased in the skin of AA mouse model. Single cell RNA sequencing and immunohistochemistry showed that RIPK1 is highly increased in dendritic cells (DCs) and CD8+ T cells. RIPK1 inhibitors (i.e., Necrostatin-1s and GSK2982772) delayed the onset of AA in mouse model, and reduced the DCs and CD8+ T cells in AA skin. RIPK1 inhibitors also increased the hair length in the mouse hair organ culture mimicking AA. Collectively, these results suggest that RIPK1 is involved in AA onset via modulating immune cells, and RIPK1 inhibitors could prevent AA onset.
Keywords
RIPK1; alopecia areata; dendritic cell; CD8+ T cell; Necrostatin-1s; GSK2982772
Subject
Biology and Life Sciences, Biology and Biotechnology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
