Notice: Users may be experiencing issues with displaying some pages on stanfordhealthcare.org. We are working closely with our technical teams to resolve the issue as quickly as possible. Thank you for your patience.
New to MyHealth?
Manage Your Care From Anywhere.
Access your health information from any device with MyHealth. You can message your clinic, view lab results, schedule an appointment, and pay your bill.
ALREADY HAVE AN ACCESS CODE?
DON'T HAVE AN ACCESS CODE?
NEED MORE DETAILS?
MyHealth for Mobile
Get the iPhone MyHealth app »
Get the Android MyHealth app »
Rebound effect associated with JAK inhibitor use in the treatment of alopecia areata. Journal of the European Academy of Dermatology and Venereology : JEADV
Gordon, S. C., Abudu, M., Zancanaro, P., Ko, J. M., Rosmarin, D.
2018
Abstract
Alopecia areata (AA) is a common autoimmune disease driven by Th1 cytokines characterized by non-scarring hair loss.1,2 Mouse models have demonstrated that IFN-gamma-producing NKG2D+ CD8+ cytotoxic T lymphocytes (CTLs) are essential for disease pathogenesis, along with JAK-STAT dependent cytokines IFN-gamma and IL-15, which induce autoreactive T cell activation.1,3 This article is protected by copyright. All rights reserved.
View details for DOI 10.1111/jdv.15383
View details for PubMedID 30520145