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CD160 inhibits activation of human CD4+ T cells through interaction with herpesvirus entry mediator

Guifang Cai1, Anukanth Anumanthan, Julia A Brown

  • 1Department of Medical Oncology, Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.

Nature Immunology
|January 15, 2008
PubMed

Insights

CD160 acts as a negative regulator in CD4+ T cell activation. Its interaction with herpesvirus entry mediator (HVEM) modulates T cell responses, inhibiting activation when HVEM is engaged by CD160 or BTLA.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Signaling

Background:

  • CD160 is a GPI-anchored immunoglobulin superfamily member found on lymphocytes.
  • Its role in T cell activation, particularly in CD4+ T cells, requires further elucidation.

Purpose of the Study:

  • To investigate the function of CD160 in human CD4+ T cell activation.
  • To identify ligands for CD160 and elucidate their role in T cell signaling.

Main Methods:

  • Flow cytometry to assess CD160 expression.
  • Monoclonal antibody crosslinking to study CD160 function.
  • Co-culture assays with HVEM-transfected cells.
  • Genetic manipulation of HVEM (deletion of cysteine-rich domain 1).

Main Results:

  • CD160 expression increases upon human CD4+ T cell activation.
  • Crosslinking CD160 inhibits CD3/CD28-mediated T cell activation.
  • Herpesvirus entry mediator (HVEM) is a CD160 ligand, acting as a bidirectional switch for T cell activation.
  • HVEM-mediated inhibition of CD4+ T cell activation depends on CD160 and BTLA.

Conclusions:

  • CD160 functions as a negative regulator of CD4+ T cell activation.
  • The CD160-HVEM interaction is critical for modulating T cell responses.
  • HVEM's interaction with CD160 and BTLA dictates the outcome of T cell activation.

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