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Immunological responses against an autologous human hepatocellular carcinoma cell line
Author(s) -
USUDA SEIICHI,
YOSHIZAWA KANAME,
YABU KOJI,
KIYOSAWA KENDO
Publication year - 1993
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.1993.tb01645.x
Subject(s) - cytotoxic t cell , lymphokine activated killer cell , lymphokine , cd8 , immunology , major histocompatibility complex , ctl* , biology , cd3 , lymphocyte , effector , natural killer t cell , interleukin 21 , immune system , cancer research , in vitro , biochemistry
We performed a detailed analysis of immune responses in a hepatocellular carcinoma (HCC) cell line and effector cells obtained from a patient with HCC. We examined the cytotoxic activity of natural killer (NK) cells, lymphokine‐activated killer (LAK) cells and cytotoxic T lymphocytes (CTL) against an autologous tumour cell line (SUHC‐1) to investigate the immune mechanism of human lymphocytes against HCC cells. Cytotoxic T lymphocytes were induced by co‐culturing of peripheral blood lymphocytes (PBL) and SUHC‐1 cells, mixed lymphocyte and tumour cell culture (MLTC). The susceptibility of SUHC‐1 to NK and LAK cells was similar to that of other allogeneic cell lines, such as K562, PLC/PRF/5 and Mahlavu. Effector cells induced in the primary MLTC had high cytotoxic acitivity but were not specific for SUHC‐1. Cytotoxic T lymphocytes with specific activity against SUHC‐1 were induced after PBL were stimulated five times at 7–10 day intervals with SUHC‐1 and low‐dose recombinant interleukin‐2 (rIL‐2), suggesting that as the culture progressed, broadly reactive effector cells disappeared and specific effector cells survived. The specific effector cells were identified as CD3 + /CD4 + and CD + /CD8 + T‐lymphocyte subsets. The recognition mechanisms of CD3 + /CD4 + CTL remain unresolved because the cytotoxicities were not inhibited by anti‐CD4 and anti‐major histocompatibility complex (MHC) class II monoclonal antibodies (MoAb). Treatment of cells with anti‐CD3, anti‐CD8 and anti‐MHC class I MoAb partially inhibited lysis. These results demonstrated that the T‐cell receptor (TCR)/CD3 complex appeared to be involved in SUHC‐1 specific antigen recognition and antigen recognition of CD3 + /CD8 + CTL was MHC class I restricted.