Publication | Open Access
Triggering of T cell proliferation through AIM, an activation inducer molecule expressed on activated human lymphocytes.
281
Citations
52
References
1988
Year
Novel Activation AntigenLymphocyte DevelopmentImmunologyImmune RegulationImmunologic MechanismAntigen ProcessingImmunotherapyActivated Human LymphocytesT Cell ProliferationCell SignalingActivation Inducer MoleculeAnti-cd3 MabAutoimmune DiseaseAllergyMab BindingAutoimmunityT Cell ImmunityCell BiologyT Cell BiologyImmunomodulationCellular Immune ResponseMedicine
In this report, we describe a novel activation antigen that appears very early after T cell activation and is absent in resting lymphocytes, through which agonistic proliferative signals can be triggered by mAb binding. It has been designated as activation inducer molecule (AIM) and is a disulphide-linked heterodimeric structure containing two polypeptide chains of Mr 33,000 and 27,000. The expression of AIM can be induced by different activation stimuli such as PMA, PHA, or anti-CD3 mAb, but not by the Ca2+ ionophore A23187, and it precedes the expression of other activation molecules such as 4F2 or the IL-2-R. Once AIM antigens are expressed on lymphocytes after stimulation with submitogenic doses of PMA, the binding of anti-AIM mAbs triggers a strong proliferative response. Furthermore, a comitogenic effect of the anti-AIM mAbs is exerted in the presence of either PHA or anti-CD3 mAb. The activation of lymphocytes through AIM antigens induces both IL-2 and IL-2-R receptor synthesis and is inhibited by anti-IL-2-R mAbs.
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