Thalidomide upregulates macrophage inflammatory protein-1alpha in a herpes simplex virus-induced Behçet's disease-like animal model.

Abstract:

:The mechanism of action of thalidomide in the treatment of patients with Behçet's disease (BD) is poorly understood. There is some evidence to suggest that certain immunological abnormalities are associated with the pathogenesis of BD. A BD-like mouse model induced by herpes simplex virus (HSV) inoculation shows similar immunological abnormalities. In this study, thalidomide was administered in order to understand the mechanism for the improvement in symptoms in BD-like mice. Eight out of ten thalidomide-treated mice showed improvement but none of ten placebo-treated mice (P < 0.005). The improvements were seen in mucocutaneous symptoms. The mice were sacrificed on the 6th day, and the spleens subjected to RT-PCR, FACS, Western blot and immunohistochemical analysis. IL-2, IL-4, IL-6, IL-10, IFN-gamma, TNFalpha, TGFbeta, MCP-1, RANTES, perforin, IP-10, FasL, FasR and MIP-lalpha were determined. Among these, TNFalpha, MIP-1alpha, perforin and Fas were influenced by thalidomide treatment. These results suggest that thalidomide can attenuate HSV-induced BD-like symptoms in mice through the downregulation of TNFalpha (P < 0.005) and the upregulation of MIP-1alpha (P < 0.005), perforin (P < 0.05) and FasR (P < 0.1).

journal_name

Arch Dermatol Res

authors

Lee ES,Kim YA,Kwon HJ,Bang D,Lee S,Sohn S

doi

10.1007/s00403-004-0498-8

keywords:

subject

Has Abstract

pub_date

2004-09-01 00:00:00

pages

175-81

issue

4

eissn

0340-3696

issn

1432-069X

journal_volume

296

pub_type

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