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Targeting of Th1-associated chemokine receptors CXCR3 and CCR5 as therapeutic strategy for inflammatory diseases.

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Targeting of Th1-associated chemokine receptors CXCR3 and CCR5 as therapeutic strategy for inflammatory diseases. / Turner, Jan Eric; Steinmetz, Oliver; Stahl, Rolf A.K.; Panzer, Ulf.

In: MINI-REV MED CHEM, Vol. 7, No. 11, 11, 2007, p. 1089-1096.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Turner, JE, Steinmetz, O, Stahl, RAK & Panzer, U 2007, 'Targeting of Th1-associated chemokine receptors CXCR3 and CCR5 as therapeutic strategy for inflammatory diseases.', MINI-REV MED CHEM, vol. 7, no. 11, 11, pp. 1089-1096. <http://www.ncbi.nlm.nih.gov/pubmed/18045212?dopt=Citation>

APA

Turner, J. E., Steinmetz, O., Stahl, R. A. K., & Panzer, U. (2007). Targeting of Th1-associated chemokine receptors CXCR3 and CCR5 as therapeutic strategy for inflammatory diseases. MINI-REV MED CHEM, 7(11), 1089-1096. [11]. http://www.ncbi.nlm.nih.gov/pubmed/18045212?dopt=Citation

Vancouver

Turner JE, Steinmetz O, Stahl RAK, Panzer U. Targeting of Th1-associated chemokine receptors CXCR3 and CCR5 as therapeutic strategy for inflammatory diseases. MINI-REV MED CHEM. 2007;7(11):1089-1096. 11.

Bibtex

@article{387db897754f4b7fa1904d1d96b04e5d,
title = "Targeting of Th1-associated chemokine receptors CXCR3 and CCR5 as therapeutic strategy for inflammatory diseases.",
abstract = "CXCR3 and CCR5 are chemokine receptor that are predominantly expressed on the surface of Th1 polarized T cells. In a variety of human and experimental autoimmune diseases the enhanced expression of CXCR3 and CCR5 binding chemokine ligands is followed by the recruitment of CXCR3- and CCR5-positive T cells, indicating an important role for these chemokine receptors in T cell-mediated tissue damage. In this review, we summarize a number of in vivo studies available on the neutralization of CXCR3 and CCR5 in inflammatory disease, and specifically focus on the potential therapeutic effects of CXCR3 and CCR5 blockade in human autoimmune disease and organ transplantation.",
author = "Turner, {Jan Eric} and Oliver Steinmetz and Stahl, {Rolf A.K.} and Ulf Panzer",
year = "2007",
language = "Deutsch",
volume = "7",
pages = "1089--1096",
journal = "MINI-REV MED CHEM",
issn = "1389-5575",
publisher = "Bentham Science Publishers B.V.",
number = "11",

}

RIS

TY - JOUR

T1 - Targeting of Th1-associated chemokine receptors CXCR3 and CCR5 as therapeutic strategy for inflammatory diseases.

AU - Turner, Jan Eric

AU - Steinmetz, Oliver

AU - Stahl, Rolf A.K.

AU - Panzer, Ulf

PY - 2007

Y1 - 2007

N2 - CXCR3 and CCR5 are chemokine receptor that are predominantly expressed on the surface of Th1 polarized T cells. In a variety of human and experimental autoimmune diseases the enhanced expression of CXCR3 and CCR5 binding chemokine ligands is followed by the recruitment of CXCR3- and CCR5-positive T cells, indicating an important role for these chemokine receptors in T cell-mediated tissue damage. In this review, we summarize a number of in vivo studies available on the neutralization of CXCR3 and CCR5 in inflammatory disease, and specifically focus on the potential therapeutic effects of CXCR3 and CCR5 blockade in human autoimmune disease and organ transplantation.

AB - CXCR3 and CCR5 are chemokine receptor that are predominantly expressed on the surface of Th1 polarized T cells. In a variety of human and experimental autoimmune diseases the enhanced expression of CXCR3 and CCR5 binding chemokine ligands is followed by the recruitment of CXCR3- and CCR5-positive T cells, indicating an important role for these chemokine receptors in T cell-mediated tissue damage. In this review, we summarize a number of in vivo studies available on the neutralization of CXCR3 and CCR5 in inflammatory disease, and specifically focus on the potential therapeutic effects of CXCR3 and CCR5 blockade in human autoimmune disease and organ transplantation.

M3 - SCORING: Zeitschriftenaufsatz

VL - 7

SP - 1089

EP - 1096

JO - MINI-REV MED CHEM

JF - MINI-REV MED CHEM

SN - 1389-5575

IS - 11

M1 - 11

ER -