| Autor: |
Kruger, M., Van Gool, S., Peng, X.H., Coorevits, L., Casteels-van Daele, M., Ceuppens, J. L. |
| Předmět: |
|
| Zdroj: |
Immunology; May96, Vol. 88 Issue 1, p49-54, 6p |
| Abstrakt: |
Granulocyte-macrophage colony-stimulating factor (GM-CSF) has proliferation- and differentiation-inducing effects on immature myeloid cells in the bone marrow, and it can modulate the function of several types of mature myeloid cells. We have stimulated purified human T cells with immobilized anti-CD3 or mitogenic anti-CD2 (a combination of monoclonal antibodies 9-1 and 9.6) which could induce GM-CSF production. The cytokines interleukin-1β (IL-1β) and IL-2 strongly enhanced GM-CSF production, while IL-4, IL-6, GM-CSF, interferon-γ (IFN-γ) and turnout necrosis factor (TNF) had no effect. Activation of protein kinase C by phorbol myristate acetate or triggering of CD28 on T cells by monoclonal antibody 9.3 provided accessory signals for enhanced GM-CSF production in activated T cells. Most important, the addition of mouse cells transfected with human B7-1 (CD80), a natural ligand for CD28, provided a potent accessory signal for GM-CSF production by activated T cells, which could not be blocked by cyclosporin A. The effect of IL-1β was in fact indirect, and resulted from enhanced IL-2 production, while the effect of B7 resulted from both IL-2-dependent and IL-2-independent pathways. We conclude that antigen-presenting cells (APC) can up-regulate GM-CSF production through IL-1β and through CD28 triggering by B7 molecules. As GM-CSF itself up-regulates B7 expression and IL-1β production by APC, a bidirectional regulatory feedback pathway between APC and T cells seems to modulate GM-CSF production. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
