caa a22 4500 469073705 CHVBK 20180323132929.0 cr unu---uuuuu 170328e19920501xx s 000 0 eng 10.1007/BF01756187 doi (NATIONALLICENCE)springer-10.1007/BF01756187 The polysaccharide K (PSK) potentiates in vitro activation of the cytotoxic function in human blood lymphocytes by autologous tumour cells [Elektronische Daten] [F. Vánky, P. Wang, E. Klein] Summary: We have studied the effect of polysaccharide K (PSK) in the in vitro recognition of ex vivo carcinoma, sarcoma and lymphoma cells by the autologous blood lymphocytes. In 4/25 experiments PSK treatment activated the lymphocytes for auto-tumour lysis. Tumour cells alone generated lytic activity both in short- (16 h) and in longterm (6 days) mixed lymphocyte/tumour cell cultures (MLTC), in 2/12 and 3/13 cases respectively. The tumours that activated the lymphocytes expressed high levels of major histocompatibility complex (MHC) class I molecules. In vitro cytokine (interferon γ and tumour necrosis factor α) treatment of the tumour cells elevated the amounts of class I antigens and the treated cells acquired stimulatory potential. When PSK was added to the MLTC, in which untreated tumour cells were used, lytic potential was induced in 9/13 short-term and in 11/12 long-term cultures. It is noteworthy that in the presence of PSK the untreated, negative or low-class-I-expressor tumours also activated the cytotoxic function of the lymphocytes in 4/5 long-term and in 6/7 short-term cultures. Even in the case of those lymphocytes that could be activated by PSK or tumour cells alone, the simultaneous exposure was more efficient. The effect of PSK was dose-dependent, being optimal at 1 µg/ml and 10 µg/ml. The presence of EDTA and/or cytochalasin B in the cytotoxic test performed with the activated effectors abrogated the lysis, indicating the requirement of contacts with the effector cells. Springer-Verlag, 1992 Polysaccharide K nationallicence Lymphocytes nationallicence Tumour cytotoxicity nationallicence Vánky F. Department of Tumor Biology, Karolinska Institute, 104 01, Stockholm 60 400, Sweden aut Wang P. Department of Tumor Biology, Karolinska Institute, 104 01, Stockholm 60 400, Sweden aut Klein E. Department of Tumor Biology, Karolinska Institute, 104 01, Stockholm 60 400, Sweden aut Cancer Immunology, Immunotherapy Springer-Verlag 35/3(1992-05-01), 193-198 0340-7004 35:3<193 1992 35 262 https://doi.org/10.1007/BF01756187 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01756187 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Vánky F. Department of Tumor Biology, Karolinska Institute, 104 01, Stockholm 60 400, Sweden aut NATIONALLICENCE 700 1- Wang P. Department of Tumor Biology, Karolinska Institute, 104 01, Stockholm 60 400, Sweden aut NATIONALLICENCE 700 1- Klein E. Department of Tumor Biology, Karolinska Institute, 104 01, Stockholm 60 400, Sweden aut NATIONALLICENCE 773 0- Cancer Immunology, Immunotherapy Springer-Verlag 35/3(1992-05-01), 193-198 0340-7004 35:3<193 1992 35 262 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer