Deficient SOCS3 and SHP-1 Expression in Psoriatic T Cells

Karsten W Eriksen; Anders Woetmann; Lone Skov; Thorbjørn Krejsgaard; Lone F Bovin; Mikkel L Hansen; Kirsten Grønbæk; Nils Billestrup; Mogens H Nissen; Carsten Geisler; Mariusz A Wasik; Niels Odum

doi:10.1038/jid.2010.6

Deficient SOCS3 and SHP-1 Expression in Psoriatic T Cells

Karsten W Eriksen, Anders Woetmann, Lone Skov, Thorbjørn Krejsgaard, Lone F Bovin, Mikkel L Hansen, Kirsten Grønbæk, Nils Billestrup, Mogens H Nissen, Carsten Geisler, Mariusz A Wasik, Niels Odum

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

39 Citationer (Scopus)

Abstract

Udgivelsesdato: 2010-Feb-4

Originalsprog	Engelsk
Tidsskrift	Journal of Investigative Dermatology
Vol/bind	130
Udgave nummer	6
Sider (fra-til)	1590-7
Antal sider	8
ISSN	0022-202X
DOI	https://doi.org/10.1038/jid.2010.6
Status	Udgivet - 2010

Adgang til dokumentet

10.1038/jid.2010.6

Citationsformater

@article{f1ca1ef01bb511df8ed1000ea68e967b,

title = "Deficient SOCS3 and SHP-1 Expression in Psoriatic T Cells",

abstract = "IFN-alpha and skin-infiltrating activated T lymphocytes have important roles in the pathogenesis of psoriasis. T cells from psoriatic patients display an increased sensitivity to IFN-alpha, but the pathological mechanisms behind the hyperresponsiveness to IFN-alpha remained unknown. In this study, we show that psoriatic T cells display deficient expression of the suppressor of cytokine signaling (SOCS)3 in response to IFN-alpha and a low baseline expression of the SH2-domain-containing protein-tyrosine phosphatase (SHP)-1 when compared with skin T cells from nonpsoriatic donors. Moreover, IFN-alpha-stimulated psoriatic T cells show enhanced activation of JAKs (JAK1 and TYK2) and signal transducers and activators of transcription. Increased expression of SOCS3 proteins resulting from proteasomal blockade partially inhibits IFN-alpha response. Similarly, forced expression of SOCS3 and SHP-1 inhibits IFN-alpha signaling in psoriatic T cells. In conclusion, our data suggest that loss of regulatory control is involved in the aberrant hypersensitivity of psoriatic T cells to IFN-alpha.Journal of Investigative Dermatology advance online publication, 4 February 2010; doi:10.1038/jid.2010.6.",

author = "Eriksen, {Karsten W} and Anders Woetmann and Lone Skov and Thorbj{\o}rn Krejsgaard and Bovin, {Lone F} and Hansen, {Mikkel L} and Kirsten Gr{\o}nb{\ae}k and Nils Billestrup and Nissen, {Mogens H} and Carsten Geisler and Wasik, {Mariusz A} and Niels Odum",

year = "2010",

doi = "10.1038/jid.2010.6",

language = "English",

volume = "130",

pages = "1590--7",

journal = "Journal of Investigative Dermatology",

issn = "0022-202X",

publisher = "nature publishing group",

number = "6",

}

TY - JOUR

T1 - Deficient SOCS3 and SHP-1 Expression in Psoriatic T Cells

AU - Eriksen, Karsten W

AU - Woetmann, Anders

AU - Skov, Lone

AU - Krejsgaard, Thorbjørn

AU - Bovin, Lone F

AU - Hansen, Mikkel L

AU - Grønbæk, Kirsten

AU - Billestrup, Nils

AU - Nissen, Mogens H

AU - Geisler, Carsten

AU - Wasik, Mariusz A

AU - Odum, Niels

PY - 2010

Y1 - 2010

N2 - IFN-alpha and skin-infiltrating activated T lymphocytes have important roles in the pathogenesis of psoriasis. T cells from psoriatic patients display an increased sensitivity to IFN-alpha, but the pathological mechanisms behind the hyperresponsiveness to IFN-alpha remained unknown. In this study, we show that psoriatic T cells display deficient expression of the suppressor of cytokine signaling (SOCS)3 in response to IFN-alpha and a low baseline expression of the SH2-domain-containing protein-tyrosine phosphatase (SHP)-1 when compared with skin T cells from nonpsoriatic donors. Moreover, IFN-alpha-stimulated psoriatic T cells show enhanced activation of JAKs (JAK1 and TYK2) and signal transducers and activators of transcription. Increased expression of SOCS3 proteins resulting from proteasomal blockade partially inhibits IFN-alpha response. Similarly, forced expression of SOCS3 and SHP-1 inhibits IFN-alpha signaling in psoriatic T cells. In conclusion, our data suggest that loss of regulatory control is involved in the aberrant hypersensitivity of psoriatic T cells to IFN-alpha.Journal of Investigative Dermatology advance online publication, 4 February 2010; doi:10.1038/jid.2010.6.

AB - IFN-alpha and skin-infiltrating activated T lymphocytes have important roles in the pathogenesis of psoriasis. T cells from psoriatic patients display an increased sensitivity to IFN-alpha, but the pathological mechanisms behind the hyperresponsiveness to IFN-alpha remained unknown. In this study, we show that psoriatic T cells display deficient expression of the suppressor of cytokine signaling (SOCS)3 in response to IFN-alpha and a low baseline expression of the SH2-domain-containing protein-tyrosine phosphatase (SHP)-1 when compared with skin T cells from nonpsoriatic donors. Moreover, IFN-alpha-stimulated psoriatic T cells show enhanced activation of JAKs (JAK1 and TYK2) and signal transducers and activators of transcription. Increased expression of SOCS3 proteins resulting from proteasomal blockade partially inhibits IFN-alpha response. Similarly, forced expression of SOCS3 and SHP-1 inhibits IFN-alpha signaling in psoriatic T cells. In conclusion, our data suggest that loss of regulatory control is involved in the aberrant hypersensitivity of psoriatic T cells to IFN-alpha.Journal of Investigative Dermatology advance online publication, 4 February 2010; doi:10.1038/jid.2010.6.

U2 - 10.1038/jid.2010.6

DO - 10.1038/jid.2010.6

M3 - Journal article

C2 - 20130595

SN - 0022-202X

VL - 130

SP - 1590

EP - 1597

JO - Journal of Investigative Dermatology

JF - Journal of Investigative Dermatology

IS - 6

ER -