Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 204, Issue 13, Pages 3183-3194Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20071094
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Funding
- NCRR NIH HHS [UL1 RR024143, UL1RR024143] Funding Source: Medline
- NIAMS NIH HHS [K23 AR052404, 1 K23 AR-052404-01A1] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007739, GM07739] Funding Source: Medline
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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 Th1 7 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.
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