Patients with a deficiency of natural killer cell activity lack the VEP13-positive lymphocyte subpopulation

Abstract

Many patients with B-type chronic lymphocytic leukemia (CLL) exhibit a profound defect in their natural killer (NK) cell activity, the basis of which is still obscure. Hence, we analyzed the NK cells from peripheral blood samples from 11 patients with CLL for phenotype and function, after removal of the leukemic cells with a monoclonal antibody (BA-1) plus complement. Phenotypic analysis of these nonleukemic cells with monoclonal antibodies (MoAbs) against NK cells revealed that the CLL patients had higher percentages of HNK-1-positive cells (23.5% compared to controls with 14.7%). In contrast, VEP13- positive cells were absent or low in seven patients (0.8% compared to controls with 11.2%) and normal in four patients (10.5%). When testing NK cell activities against K562 or MOLT 4 target cells, patients with no or minimal numbers of VEP13-positive cells were found to be deficient, while patients with normal percentages of VEP13-positive cells had NK cell activity comparable to controls. Isolation by fluorescence-activated cell sorter of HNK-1-positive cells from patients lacking VEP13-positive cells and NK cell activity indicated that the majority of the HNK-1-positive cells in these patients had the large granular lymphocyte morphology that is characteristic of NK cells. Thus, the deficiency of NK cell activity in CLL patients appears to result from the absence of cells carrying the VEP13 marker.

High interferon titer and defective NK‐cell activity in the circulation of nasopharyngeal carcinoma patients

“…5). A similar expansion of T8+/HNK-I lymphocytes has been reported in AIDS patients, in patients with chronic lymphocytic leukemia and in those with primary immunodeficiency disease (Lifson et al, 1984;Zeigler-Heitbrock et al, 1985;Huwyler et al, 1984). However, the function of these cells remains speculative.…”

Deficient production of tumor necrosis factor by peripheral‐blood monocytes in chronic lymphocytic leukemia

“…Decreased activity of TNF (and in addition to IL-1, Rossi et al, 1985) could also have implications for hypogammaglobulinemia of CLL patients (Rundles et al, 1954;Foa et al, 1979;Ben-Bassat et al, 1979), since these monokines regulate Bcell function. In addition, both impaired TNF production and deficient NK cell activity observed in CLL (Ziegler et al, 1981;Kay and Zarling, 1984;Ziegler-Heitbrock et al, 1985) could be responsible for the increased incidence of secondary malignancies in CLL (Manusow and Weinerman, 1975;Greene et al, 1978;Davis et al, 1987). Since TNF stimulates the production of hemopoietic CFSs by fibroblasts and monocytes, a deficiency of both monokines may result in a deficiency in CSFs and thus contribute to impaired hematopoiesis.…”

“…The response of purified T lymphocytes to mitogens is decreased and allogeneic as well as autologous mixed lymphocyte reactions are impaired (Cone and Uhr, 1964;Block et al, 1969). Natural killer cell (NK) activity is reduced, and a lack of CD16+ NK cells is also observed (Ziegler et al, 1981;Kay and Zarling, 1984;Ziegler-Heitbrock et al, 1985). Decreased T-helper-cell activity and increased T-suppressor-cell activity has been observed (Chiorazzi et al, 1979;Kay, 1981;Perri and Kay, 1986) with increased absolute numbers of T8+ cells in peripheral blood (Catovsky et al, 1974;Kay et al, 1979;Platsoucas et al, 1982).…”

Ο Ρολος Των Cd8 Λεμφοκυτταρων Στην Εμφανιση Ουδετεροπενιας Στους Πασχοντες Απο Χρονια Β-Λεμφοκυτταρικη Λευχαιμια

“…Ο αριθμός τους έχει αναφερθεί ελαττωμένος, φυσιολογικός ή αυξημένος [26,135,137,138]. [136,138] καθιστά απίθανο το ενδε-χόμενο συμμετοχής των κυττάρων αυτών στον καθορισμό της ουδετεροπενίας στους αρρώστους μας.…”