Serum-soluble Herpes Virus Entry Mediator Levels Reflect Disease Severity and Th2 Environment in Cutaneous T-cell Lymphoma
Tomomitsu Miyagaki, Makoto Sugaya*, Hiraku Suga, Hanako Ohmatsu, Hideki Fujita, Yoshihide Asano, Yayoi Tada, Takafumi
Kadono and Shinichi Sato
Department of Dermatology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. *E-mail: email@example.com
Activated T cells express LIGHT, an acronyme for lymphotoxin-like, exhibits inducible expression, and competes with HSV glycoprotein D for herpesvirus entry mediator (HVEM) a receptor expressed by T lymphocytes (1). LIGHT binds to 3 distinct receptors: HVEM, lymphotoxin β receptor, and decoy receptor 3 (2). Of these, HVEM is expressed by many cell types (1). LIGHT-HVEM interactions activate T cells and natural killer (NK) cells to produce T helper type (Th) 1 cytokines (3–7).
Many patients with cutaneous T-cell lymphoma (CTCL) in the advanced stages have eosinophilia and high levels of immunoglobulin E, suggesting that Th2 is dominant in these patients (8, 9).
We reported recently that low HVEM expression on dermal fibroblasts in lesional skin of advanced CTCL attenuates the expression of Th1 chemokines, which may contribute to a shift to a Th2-dominant microenvironment (10). However, little is known about the soluble
form of HVEM (sHVEM) and its ligand, LIGHT, in CTCL. The aim of this study was to measure sHVEM and LIGHT levels in the sera of patients with CTCL.
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