Role of interleukin-2 (IL-2) and IL-2 receptor expression in the proliferative defect observed in mitogen-stimulated lymphocytes from patients with gliomas.
Patients with primary malignant brain tumors manifest, as previously demonstrated, a variety of abnormalities in cell-mediated and humoral immunity. Diminished lymphocyte reactivity has been recently shown in these patients to be linked to deficiencies in interleukin-2 (IL-2) production. In the present study, this observation was expanded by demonstrating that exogenous purified or recombinant IL-2 does not improve the mitogen responsiveness of lymphocytes obtained from these patients. Studies were also conducted to determine the percentage of IL-2-receptor-positive cells at various times after phytohemagglutinin stimulation with the use of anti-TAC monoclonal antibody. The results demonstrated that the number of lymphocytes induced to express receptors for IL-2 was reduced as compared to normal values. These cumulative data therefore suggest that the failure of mitogen to induce blastogenesis in lymphocytes from patients with malignant gliomas results from intrinsic deficiencies in potentially responsive cells, which are expressed in the early phase of the cell cycle.[1]References
- Role of interleukin-2 (IL-2) and IL-2 receptor expression in the proliferative defect observed in mitogen-stimulated lymphocytes from patients with gliomas. Elliott, L., Brooks, W., Roszman, T. J. Natl. Cancer Inst. (1987) [Pubmed]
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