Résumé
CD2-CD48 interactions enhance T cell receptor-driven mouse T lymphocyte activation. However, the mechanism is not well understood. Here we show that blockade of CD2-CD48 interactions with anti-CD48 monoclonal antibody (mAb) inhibited interleukin (IL)-2 and interferon (IFN)-γ expression, as well as T cell proliferation in response to mitogenic anti-CD3 mAb, although more potent inhibition resulted from blocking CD28-CD80/CD86 interactions. Blockade of both CD2 and CD28 costimulation abrogated T cell proliferation and cytokine synthesis. Conversely, T cells stimulated with immobilized anti-CD3 and anti-CD2 mAb exhibited increased proliferation and IL-2 and IFN-γ expression, although a stronger enhancing effect was obtained with immobilized anti-CD3 and anti-CD28 mAb. Concurrent CD2 and CD28 costimulation caused a further increase in proliferation and cytokine synthesis. Stimulation of purified T cells with microsphere-immobilized anti-CD3 and anti-CD2 mAb increased IL-2 and IFN-γ mRNA stability. However, CD28 costimulation had a stronger enhancing effect on IL-2 and IFN-γ mRNA stability that was not further increased by concomitant CD2 signaling. CD2, therefore, costimulates T cell activation by stabilizing cytokine mRNA transcripts, albeit with less efficiency than CD28.
Langue d'origine | English |
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Pages (de-à) | 1-12 |
Nombre de pages | 12 |
Journal | Cellular Immunology |
Volume | 229 |
Numéro de publication | 1 |
DOI | |
Statut de publication | Published - mai 2004 |
Note bibliographique
Funding Information:This work was supported by a grant to D.H. from the Natural Sciences and Engineering Research Council of Canada (NSERC). B.M. and M.H. were recipients of postgraduate scholarships from NSERC and the Killam Trust Foundation. C.W. was supported by a postgraduate scholarship from the Nova Scotia Health Research Foundation.
ASJC Scopus Subject Areas
- Immunology