Dissociation of autologous and allogeneic mixed lymphocyte reactivity by using a monoclonal antibody specific for human T helper cells.
Open Access
- 1 November 1983
- journal article
- research article
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 131 (5) , 2323-2327
- https://doi.org/10.4049/jimmunol.131.5.2323
Abstract
A monoclonal antibody defining a population of human T helper cells was developed and shown to specifically block the autologous mixed lymphocyte reaction (AMLR). This antibody, termed KT69-7 (IgG1), recognized 62% of peripheral blood E rosette-positive (E+) cells while demonstrating negligible reactivity with E- cells, monocytes, granulocytes, EBV-transformed B cell lines, and mouse splenocytes. Separation of E+ cells into KT69-7+ and KT69-7- populations revealed that KT69-7+ T cells provided helper function in PWM-driven B cell differentiation, whereas KT69-7- T cells provided no help and may suppress this response. Modulation of membrane moieties by using KT69-7 or OKT4 plus goat anti-mouse IgG removed reactivity to both these antibodies, suggesting an association between these molecules recognized by these antibodies. In functional studies, KT69-7 selectively blocked the AMLR while demonstrating minimal or no effect on the allogeneic MLR (allo-MLR). Blocking of the autoreactivity occurred when either autologous B lymphocytes or macrophages were used as stimulators. The failure of KT69-7 to block the allo-MLR was not attributable to excessive allogeneic stimulus; KT69-7 failed to block even under conditions of limiting numbers of stimulator cells. KT69-7 thus appears to recognize a molecule on the surface of T helper cells required for recognition of autologous class II antigens.This publication has 20 references indexed in Scilit:
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