Study performed on 192 patients has demonstrated that the progression rate of chronic lymphocytic leukemia (CLL) is associated with the existence of T-cell defect(s). A dynamic classification system based on evaluation of tumor mass growth rate, response to therapy, and myelopoietic failure (MF) has been devised for evaluation of progression rate of CLL. Besides four basic groups (Group 1: CLL without therapy; Group 2: CLL on therapy, without remission; Group 3: CLL on therapy, partial remission; Group 4: CLL on therapy, complete remission) patients were further classified into phase (type) A (stable, indolent CLL) or phase (type) B (active, progressive CLL). The major criteria for phase A were: total tumor mass (TTM) doubling time (DT) longer than 12 months, no MF, and/or good response to therapy. The major criteria for phase B were: TTM DT less than 12 months and/or accompanying MF and/or no response to therapy. The following major findings have been demonstrated: (1) altered quantitative relationship between active and nonactive parts of T-cell compartment (E/A ratio) in the progressive phase of CLL; (2) altered B/T gamma ratio in the progressive phase of CLL; (3) more than 50% increased percentage of T gamma cells in the stable phase of CLL; (4) very low stable and absent seeding efficiency of T-cells in the progressive phase of CLL; (5) altered (delayed) DNA synthesis pattern in the progressive phase of CLL; and (6) negative local xenogeneic graft versus host reaction in the progressive phase of CLL. Based on reported results, a hypothesis regarding the possible role of T-cells in the pathogenesis of CLL was suggested.
Cell-free peritoneal washings (PW) were collected from mice with Ehrlich ascitic carcinoma at various time intervals after tumor transplantation and tested on the immunosuppressive activity in vitro. Two assays were used: (1) stimulation of human peripheral blood lymphocytes by phytohemagglutinin (PHA) and (2) inhibition of human leukocyte migration with PPD. Fluids collected in the early phase of tumor growth (up to day 6) were ineffective, or weakly suppressive, and those collected in advanced and terminal stages of carcinoma development, were suppressive in both tests applied. Control cell-free peritoneal washings obtained from normal mice without the tumor exerted suppressive activity when adjusted to the same protein concentration as the PW from mice with Ehrlich carcinoma. This suggests that host's cells in tumor-bearing animals, rather than tumor cells themselves, may be responsible for the production of inhibitory substance(s). Cell-free peritoneal washings were also tested on their ability to influence the growth of Ehrlich carcinoma cells in vitro, as measured by 3H-thymidine incorporation. Samples collected from mice with advanced tumors stimulated the growth of tumor cells.
The dynamics of changes in the metabolic and functional activities of thymus, lymph node and spleen lymphocytes and spleen macrophages of AKR mice was examined during the preleukemic period. The MTT colorimetric assay was used to determine the mitochondrial enzyme activity of viable cells, the local xenogeneic GVH reaction and the IL-2 assay for measuring T cell responses, and the IL-1 assay as an indicator of macrophage activity. In the early preleukemic period (at 1.5 months of age), lymphocyte dehydrogenase enzyme hyperactivity was accompanied by a highly increased production of IL-2, positive local xenogeneic GVH reaction and increased IL-1 production. Later on, at the age of 4-5 months, AKR mice demonstrated a progressive decrease in the metabolic activity of lymphocytes, negative local GVH reaction and reduction or lack in IL-2 and IL-1 production. This early hyperreactivity and late, gradually evolving, areactivity of lymphocytes and macrophages was not found in other, non-leukemic strains of mice (RFM, CBA, C57BL).
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