Abstract
The proliferative response of T-cells to autologous non-T-cells is referred to as the autologous mixed lymphocyte reaction (AMLR). Recent studies have suggested that AMLR represents a mechanism of immune regulationin vivo. We investigated AMLR in patients with acute- and chronic myeloid leukemia (AML and CML). AMLR was found to be significantly depressed (P<0.001) in AML patients (n=17, cpm=532±95) and CML patients (n=13, cpm=688±99) when compared with that of their healthy HLA-identical siblings serving as controls (n=17, cpm=4152±619 and n=13 cpm=4086±421, respectively). In order to understand the cellular basis of the defective AMLR in patients with AML and CML, we performed mitogen-treated T-cell cultures analysis of T-cell subsets and HLA-II antigen detection on monocytes. The results indicated that the defect of AMLR in patients resided at the stimulator monocyte level rather than at the responder T-cell level. Enumeration of monocytes reactive with monoclonal antibody Tü22, which recognizes determinants of HLA-DQ, demonstrated that ML patients had a significantly decreased (P<0.001) number of circulating Tü22+ monocytes when compared with normal controls. These studies suggest that a deficiency of HLA-DQ+ monocytes contributes to the depression of AMLR in ML and possibly underlies the abnormalities of immune response present in this disease.
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Feili, G., Grosse Wilde, H. Impaired autologous mixed lymphocyte reaction correlated with decreased expression of HLA-I antigens on monocytes in patients with myeloid leukemia. Chinese Journal of Cancer Research 3, 11–17 (1991). https://doi.org/10.1007/BF02671284
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DOI: https://doi.org/10.1007/BF02671284