CD2 Regulates T Cell-Dependent Induction of Monocyte IL-1beta mRNA during Anti-CD3 Mitogenesis

ISSN： 0008-8749

Source： Cellular Immunology, Vol.170, Iss.1, 1996-05, pp. : 120-126

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Abstract

The induction of monocyte IL-1 mRNA during T cell activation requires that monocytes receive contact-dependent signals from activated T cells. Furthermore, the ability of T cells to induce IL-1beta mRNA is not constitutive but rather is rapidly acquired (<30 min) following activation via mechanisms that do not require protein synthesis. The goal of these studies is to identify the T cell signal(s) that mediates the cell contact-dependent induction of monocyte IL-1beta mRNA. The induction of IL-1beta mRNA during anti-CD3 mitogenesis was significantly inhibited by anti-CD2 mAb, whereas mAb against CD11a, CD18, CD69, or CD5 molecules had no effect. The inhibition of IL-1beta mRNA induction by anti-CD2 mAb was restricted to only those mAb that block CD2/CD58(LFA-3) interactions. Furthermore, anti-CD2 blocked the induction of monocyte IL-1beta mRNA by T cells that were preactivated using either immobilized anti-CD3 or anti-T11 2 plus anti-T11 3 mAb, thereby indicating that the inhibition of IL-1beta mRNA was not due to negative signaling effects exerted on the T cell by anti-CD2. Finally, although anti-CD69 mAb had no effect on IL-1beta mRNA induction, it inhibited the generation of soluble IL-1beta. The combination of anti-CD69 and anti-CD2 mAb exhibited greater inhibition of secreted IL-1beta than either antibody alone. These results indicate that CD2 is required for T cell induction of IL-1beta mRNA through interaction with LFA-3 on the monocyte and that the generation of soluble IL-1beta is regulated by CD69.