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.
 

See our updated masking policy »

Stanford Health Care

Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses JOURNAL OF EXPERIMENTAL MEDICINE Zaba, L. C., Cardinale, I., Gilleaudeau, P., Sulhvan-Whalen, M., Suarez-Farinas, M., Fuentes-Duculan, J., Novitskaya, I., Khatcherian, A., Bluth, M. J., Lowes, M. A., Krueger, J. G. 2007; 204 (13): 3183-3194

Abstract

Biological agents have dramatically improved treatment options for patients with severe psoriasis. Etanercept (tumor necrosis factor [TNF] receptor-immunoglobulin fusion protein) is an effective treatment for many psoriasis patients, and blockade of TNF is considered to be its primary action. However, in this clinical trial, we show that etanercept has early inhibitory effects on a newly appreciated type of T cells: T helper type 17 (Th17) cells. Etanercept reduced the inflammatory dendritic cell products that drive Th17 cell proliferation (interleukin [IL] 23), as well as Th17 cell products and downstream effector molecules (IL-17, IL-22, CC chemokine ligand 20, and beta-defensin 4). In contrast, Th1 cellular products and effector molecules (interferon gamma, lymphotoxin alpha, and myxovirus resistance 1) were reduced late in disease resolution. This study suggests a role for Th17 in addition to Th1 cells in the pathogenesis of psoriasis. Th17 cells may be particularly important in driving epidermal activation in psoriatic plaques, whereas Th1 cells must also be eliminated for final disease resolution.

View details for DOI 10.1084/jem.20071094

View details for Web of Science ID 000252153100015

View details for PubMedID 18039949

View details for PubMedCentralID PMC2150965