Regulation by anti-CD2 monoclonal antibody of the activation of a human T cell clone induced by anti-CD3 or anti-T cell receptor antibodies

• Published in: The Journal of immunology (1950) Vol. 139; no. 9; pp. 2850 - 2855
• Main Authors: Yssel, H, Aubry, JP, de Waal Malefijt, R, de Vries, JE, Spits, H
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 01.11.1987; American Association of Immunologists
• Subjects: Analysis of the immune response. Humoral and cellular immunity; Antibodies, Monoclonal - immunology; Antigen-Antibody Reactions; Antigens, Differentiation, T-Lymphocyte - immunology; Antigens, Surface - immunology; Biological and medical sciences; Cell Line; Epitopes; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Gene Expression Regulation; Humans; Immunobiology; Interleukin-2 - biosynthesis; Interleukin-2 - genetics; Lymphocyte Activation; Organs and cells involved in the immune response; Receptors, Antigen, T-Cell - physiology; Receptors, Immunologic - metabolism; Receptors, Interleukin-2; RNA, Messenger - genetics; T-Lymphocytes - immunology; Time Factors; Tumor Necrosis Factor Receptor Superfamily, Member 7; Antigen; Human; Membrane receptor; Immune response; Induction; T-Lymphocyte; Activation; Immune regulation; Monoclonal antibody; Clone
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.139.9.2850

In this study the effect of anti-cluster designation (CD) 2 monoclonal antibodies (mAb) on the activation of a cloned human T cell line, HY837, after triggering the CD3/T cell receptor (TcR) complex by anti-CD3 or anti-TcR mAb is described. HY837, which reacts with a series of mAb directed at different epitopes on the TcR, could be induced to proliferation and interleukin 2 (IL-2) production by soluble mAb directed at the CD3/TcR complex in the absence of accessory cells. mAb directed at the CD2 epitope T11-1 were shown to block the IL-2 production by HY837, as well as the expression of the IL-2 receptor, induced by anti-CD3 mAb, resulting in the inhibition of the proliferative response. The effect of anti-CD2 mAb on the proliferative response of HY837, induced by anti-CD3 mAb, was not due to a competition for Fc binding sites. In contrast, the proliferative responses and IL-2 production of HY837, induced by mAb directed at the TcR, were shown to be enhanced by the action of the anti-CD2 mAb. These results indicate that effects mediated by anti-CD3/TcR mAb cannot always be extrapolated to antigen-mediated effects and show that anti-CD2 mAb may regulate the T cell response, induced by mAb directed at the CD3/TcR complex, depending on which part of this complex is triggered during activation.