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HLA‐B5‐restricted auto‐tumor‐specific cytotoxic T cells generated in mixed lymphocyte‐tumor‐cell culture
Author(s) -
Wang P.,
Végh Zs.,
Vánky F.,
Klein E.
Publication year - 1992
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910520403
Subject(s) - biology , cytotoxic t cell , cd8 , lymphocyte , t lymphocyte , immunology , tumor infiltrating lymphocytes , antigen , antibody , human leukocyte antigen , tumor antigen , cancer research , immunotherapy , in vitro , immune system , biochemistry
Abstract T‐cell‐enriched lymphocyte populations derived from the malignant exudate of a patient with ovarian carcinoma were exposed to autologous tumor cells in the mixed lymphocyte‐tumor‐cell culture (MLTC) and propagated for 42 days. Proliferation of lymphocytes depended on exposures to autologous tumor cells and on the presence of IL‐2. After 7 days, the MLTC‐lymphocytes lysed K562 and the autologous tumor cells. The latter effect was not inhibited by monoclonal antibodies (MAbs) reactive with MHC class‐1 antigens or with CD3. After 7 restimulations, the culture was enriched in CD8 + cells (92%) and showed selective lytic activity against the autologous tumor. This function was inhibited by the α‐class 1 or α‐CD3 MAbs, and also by antibodies reactive with the HLA B locus or B5 allele products. The antibodies reactive with HLA A molecules had no such effect. It seems therefore that the function of the CTLs was restricted by HLA B5. Analysis of the TCRβ genes indicated clonal T‐cell expansion in this culture. This MLTC was I of 21 initiated with 11 blood‐and 10 tumor‐derived lymphocyte (TIL) populations prepared from the malignant effusions of ovarian carcinoma patients. None of these ex‐vivo lymphocytes lysed autologous tumor cells. In 17 MLTCs the lymphocytes did not proliferate, and in 3 cultures the proliferation was maintained only for 2–3 weeks. In 3 of 4 cultures auto‐tumor cytotoxicity was induced. © 1992 Wiley‐Liss, Inc.