Article abstract
Nature Immunology 9, 176 - 185 (2008)
Published online: 13 January 2008 | Corrected online: 19 March 2008 | doi:10.1038/ni1554
There is a Corrigendum (May 2008) associated with this Article.
CD160 inhibits activation of human CD4+ T cells through interaction with herpesvirus entry mediator
Guifang Cai1, Anukanth Anumanthan1, Julia A Brown1, Edward A Greenfield1, Baogong Zhu1 & Gordon J Freeman1
Abstract
CD160, a glycosylphosphatidylinositol-anchored member of the immunoglobulin superfamily, is expressed on both cytolytic lymphocytes and some unstimulated CD4+ T cells. Here we show that CD160 expression was increased after activation of human CD4+ T cells and that crosslinking CD160 with monoclonal antibody strongly inhibited CD3- and CD28-mediated activation. We found that herpesvirus entry mediator (HVEM) was a ligand of CD160 that acted as a 'bidirectional switch' for T cell activation, producing a positive or negative outcome depending on the engagement of HVEM by CD160 and known HVEM ligands such as B and T lymphocyte attenuator (BTLA) and the T lymphocyte receptor LIGHT. Inhibition of CD4+ T cell activation by HVEM-transfected cells was dependent on CD160 and BTLA; when the cysteine-rich domain 1 of HVEM was deleted, this inhibition was lost, resulting in strong T cell activation. CD160 thus serves as a negative regulator of CD4+ T cell activation through its interaction with HVEM.
- Department of Medical Oncology, Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.
Correspondence to: Gordon J Freeman1 e-mail: gordon_freeman@dfci.harvard.edu
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