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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1981 Aug;78(8):5096–5098. doi: 10.1073/pnas.78.8.5096

Monoclonal antibody analysis of human T lymphocyte subpopulations exhibiting autologous mixed lymphocyte reaction.

N K Damle, J A Hansen, R A Good, S Gupta
PMCID: PMC320339  PMID: 6458039

Abstract

In autologous mixed lymphocyte reaction (MLR), T cells proliferate in response to the stimulation by autologous non-T cells. In the present study, human T cell subpopulations, defined by murine monoclonal antibodies OKT4, OKT8, or 9.3, were examined for their capacity to proliferate in autologous and allogeneic MLR. It was observed that the treatment of responder T cells with OKT4 or 9.3 antibody (both defining helper/inducer T cells) and complement (C') ablated their proliferative response in autologous MLR and markedly reduced their allogeneic MLR proliferative response. In contrast, treatment of T cells with OKT8 antibody (defining suppressor/cytotoxic T cells) and C' had no or minimal effect on their proliferative response in autologous MLR. Furthermore, OKT4, 9.3, 9.6 (PAN), or 7.2 anti-human Ia (framework specific) but OKT8 antibody, when present during the entire culture period, in the absence of C' inhibited in a dose-dependent manner the proliferative response in both autologous and allogeneic MLR. Inhibition of proliferation was also observed when the responder T cells were pretreated with OKT4 or 9.3 antibody, washed, and then stimulated with irradiated autologous or allogeneic non-T cells. Pretreatment of T cells with OKT8 or 7.2 anti-Ia antibody in the absence of C' did not influence their proliferative response in autologous MLR. Thus, T cells containing cells with helper/inducer activity defined by OKT4 or 9.3 antibody appear to be the major responder T-cell subpopulation in autologous MLR.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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