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Human T cell responses to IL-1 and IL-6 are dependent on signals mediated through CD2
B Endler-Jobst1, B Schraven, B Hutmacher
1Abtlg. Angewandte Immunologie, Deutsches Krebsforschungszentrum, Heidelberg, Federal Republic of Germany.
We investigated the involvement of IL-1 and IL-6 in activation of resting human T lymphocytes via the Ti-Ag receptor/CD3-dependent and the CD2-dependent pathways, respectively. When lymphocytes were triggered through CD3-Ti, neither IL-1 nor IL-6 nor the combination of both cytokines was capable of inducing a proliferative response, whereas addition of monocytes or IL-2 to such a system mediated DNA synthesis and cellular mitosis. In contrast, in the presence of submitogenic concentrations of mAb directed at CD2, IL-1 and/or IL-6 produced marked comitogenic dose-dependent effects. Moreover, although the action of IL-1 was clearly dependent on expression of the IL-2/IL-2R system, proliferation to CD2 antibody plus IL-6 could not be blocked by mAb directed at the IL-2R and/or IL-4. T cell responsiveness to both IL-1 and IL-6 was facilitated in the presence of CD58-like signals as delivered by human rCD58, SRBC or a mAb (anti-T111A), which binds to an interaction site for CD58 on the human CD2 molecule. These findings indicate that CD2 and its ligand CD58 play an important role in T cell/monocyte interactions during primary immune responses by means of upregulating T cell susceptibility to monocyte-derived cytokines.
We investigated the involvement of IL-1 and IL-6 in activation of resting human T lymphocytes via the Ti-Ag receptor/CD3-dependent and the CD2-dependent pathways, respectively. When lymphocytes were triggered through CD3-Ti, neither IL-1 nor IL-6 nor the combination of both cytokines was capable of inducing a proliferative response, whereas addition of monocytes or IL-2 to such a system mediated DNA synthesis and cellular mitosis. In contrast, in the presence of submitogenic concentrations of mAb directed at CD2, IL-1 and/or IL-6 produced marked comitogenic dose-dependent effects. Moreover, although the action of IL-1 was clearly dependent on expression of the IL-2/IL-2R system, proliferation to CD2 antibody plus IL-6 could not be blocked by mAb directed at the IL-2R and/or IL-4. T cell responsiveness to both IL-1 and IL-6 was facilitated in the presence of CD58-like signals as delivered by human rCD58, SRBC or a mAb (anti-T111A), which binds to an interaction site for CD58 on the human CD2 molecule. These findings indicate that CD2 and its ligand CD58 play an important role in T cell/monocyte interactions during primary immune responses by means of upregulating T cell susceptibility to monocyte-derived cytokines.