Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses.
Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses.
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通过TNF抑制来改善表皮增生与TH17反应减少有关。
DOI:
10.1084/jem.20071094
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发表时间:
2007-12-24
期刊:
影响因子:
--
通讯作者:
Krueger JG
中科院分区:
文献类型:
--
作者:
Zaba LC;Cardinale I;Gilleaudeau P;Sullivan-Whalen M;Suárez-Fariñas M;Fuentes-Duculan J;Novitskaya I;Khatcherian A;Bluth MJ;Lowes MA;Krueger JG
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 β-defensin 4). In contrast, Th1 cellular products and effector molecules (interferon γ, lymphotoxin α, 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.
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影响因子:
82.9
作者:
Conrad, Curdin;Boyman, Onur;Nestle, Frank O.
通讯作者:
Nestle, Frank O.
DOI:
10.1084/jem.20070663
发表时间:
2007-08-06
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Annunziato F;Cosmi L;Santarlasci V;Maggi L;Liotta F;Mazzinghi B;Parente E;Filì L;Ferri S;Frosali F;Giudici F;Romagnani P;Parronchi P;Tonelli F;Maggi E;Romagnani S
通讯作者:
Romagnani S
影响因子:
4.4
作者:
Kao, CY;Chen, Y;Wu, R
通讯作者:
Wu, R
影响因子:
4.6
作者:
Arican O;Aral M;Sasmaz S;Ciragil P
通讯作者:
Ciragil P
影响因子:
10.3
作者:
Lew, W;Lee, E;Krueger, JG
通讯作者:
Krueger, JG