“…The effector cells involved are probably heterogeneous, dependent upon the species investigated, the types of target cells and the assays employed. More than one mechanism is also probably involved since there is evidence for both antibodydependent and antibody-independent natural killing (Kall and Koren, 1979).…”
A major distinction is reported between the cytolytic activity of peripheral blood lymphocytes (PBL) and that of lymph-node and tumour-infiltrating lymphocytes (TIL) against targets of the NK-sensitive K562 cell line in short-term 51Cr release assays. In the PBL of normal donors and lung cancer patients in whom disease was advanced anti-K562 reactivity, though variable, was consistently detectable and this activity could be augmented to a similar extent in patients and controls by treatment of effectors with exogenous interferon (IF). By contrast anti-K562 activity in lymph-node cells (LNC) and TIL was virtually absent and significant levels could not be induced by exposure to IF. This activity was not attributable to coexistent suppressor cells for NK function since admixture of LNC and TIL with normal PBL failed to modulate K562 killing by the latter. The results imply that K562-reactive NK cells and their precursors may frequently be present at sub-threshold levels in the lymph nodes of tumour-bearing patients and a similar explanation could account for the inactivity of TIL. However, in the latter situation, actively-induced NK dysfunction in situ incapable of regeneration by IF, and attributable to as yet undefined tumour-associated factors, may also be involved.
“…The effector cells involved are probably heterogeneous, dependent upon the species investigated, the types of target cells and the assays employed. More than one mechanism is also probably involved since there is evidence for both antibodydependent and antibody-independent natural killing (Kall and Koren, 1979).…”
A major distinction is reported between the cytolytic activity of peripheral blood lymphocytes (PBL) and that of lymph-node and tumour-infiltrating lymphocytes (TIL) against targets of the NK-sensitive K562 cell line in short-term 51Cr release assays. In the PBL of normal donors and lung cancer patients in whom disease was advanced anti-K562 reactivity, though variable, was consistently detectable and this activity could be augmented to a similar extent in patients and controls by treatment of effectors with exogenous interferon (IF). By contrast anti-K562 activity in lymph-node cells (LNC) and TIL was virtually absent and significant levels could not be induced by exposure to IF. This activity was not attributable to coexistent suppressor cells for NK function since admixture of LNC and TIL with normal PBL failed to modulate K562 killing by the latter. The results imply that K562-reactive NK cells and their precursors may frequently be present at sub-threshold levels in the lymph nodes of tumour-bearing patients and a similar explanation could account for the inactivity of TIL. However, in the latter situation, actively-induced NK dysfunction in situ incapable of regeneration by IF, and attributable to as yet undefined tumour-associated factors, may also be involved.
“…Furthermore, Klein (17) found no difference in the kinetics of killing between K and NK cells, when using the 331 same target cells. Kall (15) believes that the cells involved in natural killing which are non T, non B, non macrophage and Fc receptor positive cells, bear a close resemblance to the K cells and she could detect (16) both serum dependent and serum independent NK cells. Our results show pre-operatively impaired SLMC and ADCC in glioma patients when compared both with healthy controls, bladder and kidney cancer patients.…”
The authors studied 24 patients affected by anaplastic gliomas in regard to the killer (Antibody-Dependent Cellular Cytotoxicity) and natural killer (Spontaneous Lymphocyte-Mediated Cytotoxicity) immunological functions, by counting the Cr51 release in Change liver and K 562 cell cultures, respectively. These parameters were also evaluated in 24 healthy donors as control, in 24 patients affected by bladder cancer and in nine cases of kidney cancer. Our data show, pre-operatively, a statistically significant impairment of ADCC and SLMC activity in glioma patients as compared both with controls, bladder and kidney cancer patients. The particular impairment of K and NK functions in gliomas is discussed with regard to the specific features of Central Nervous System malignancies. An improvement of ADCC activity was also found in the post-operative samples. This finding confirms other reports about partial restoring of altered immunocompetence after surgery, suggesting a link between extention of tumor mass and impaired immunological reactions.
“…This observation, and the demonstration of the ubiquity of serum natural anti-tumor antibodies, suggests that K-cell ADCC based on natural antibodies may be one mechanism of natural resistance. In fact, this theory has led several investigators to test the hypothesis that natural killer (NK) cells are K cells armed in vivo by natural antibodies (Koide and Takasugi, 1977;Troye et al, 1977;Kay et al, 1979;Kall and Koren, 1979;Pape et al, 1979), and although the weight of evidence does not favor the idea that NK-cell activity is antibody-mediated, there is evidence in humans that in vivo armed K cells can be lytic for tumor cells in vitro (Kall and Koren, 1979;Pape et al, 1979).…”
The objective of this study was to investigate whether natural anti-tumor antibodies (NAb) contributed to the surveillance of small inocula of syngeneic tumors. Experiments were designed to distinguish between NAb and NK-mediated host resistance. Four approaches were used: (1) the isolation of tumor variants differing in their tumorigenicity and susceptibility to these mechanisms, and to activated macrophages; (2) a comparison of the effects of adjuvants on the modification of both host resistance and the activity of these effectors; (3) the relationship between the ontogeny of the natural resistance mechanisms and tumorigenicity in aged mice; and (4) the use of a Winn-type assay. These studies provided support for a role in natural resistance correlated with both the ability of tumors to bind NAb, and the production of NAb in adjuvant-stimulated mice. Furthermore, the frequency of tumors observed after tumor challenge more closely correlated with the ontogeny of natural antibody than NK cells, and tumors coated with NAb were less tumorigenic than controls. The reduced tumorigenicity of an NK-sensitive tumor, when compared to an NK-resistant variant of the same line, provided evidence for NK-cell-mediated natural resistance in young adult mice. It was concluded that natural resistance to tumors is a complex phenomenon dependent on the tumor phenotype, as well as the activity of several effector mechanisms, and that natural anti-tumor antibody must be considered an important component of host resistance.
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