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Cytotoxic T‐cell clone against rectal carcinoma induced by stimulation of a patient's peripheral blood mononuclear cells with autologous cultured tumor cells
Author(s) -
Jacob Lutz,
Somasundaram Rajasekharan,
Smith William,
Monos Dimitrios,
Basak Saroj,
Marincola Francesco,
Pereira Sarita,
Herlyn Dorothee
Publication year - 1997
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/(sici)1097-0215(19970502)71:3<325::aid-ijc3>3.0.co;2-#
Subject(s) - ctl* , clone (java method) , cytotoxic t cell , peripheral blood mononuclear cell , immunology , immunotherapy , biology , medicine , antigen , cancer research , cd8 , immune system , in vitro , dna , biochemistry , genetics
In an effort to establish cytolytic T lymphocytes (CTLs) against colorectal carcinoma (CRC) by stimulating patients' lymphocytes with autologous tumor cells, we used peripheral blood mononuclear cells (PBMC) from a patient with minimal residual rectal carcinoma following removal of the primary lesion and involved regional lymph nodes as a source to generate CTLs in culture. A CTL line and clone were established from the patient's PBMC following stimulation of PBMC with autologous, cultured tumor cells and interleukin‐2. The CTL line and the clone consisted predominantly of CD4 + lymphocytes. The CTL clone expressed two T‐cell receptor variable α chains (Vα11 and Vα22) and one β chain (Vβ14). The cytokine secretion pattern of the CTL line was of the Th1‐type. Both the CTL line and the clone lysed the autologous rectal carcinoma cells, but not the allogeneic, partially human lymphocyte antigen (HLA)‐matched or nonmatched CRC cells, autologous Epstein‐Barr virus‐transformed B cells, K562 (natural killer target) cells or Daudi (lymphokine‐activated killer target) cells. Lysis of autologous tumor cells most likely was HLA class I‐restricted. Our unique success in generating CTLs against this tumor type may rest in the inclusion of a patient with minimal residual, rather than advanced, disease. Int. J. Cancer 71:325‐332, 1997. © 1997 Wiley‐Liss Inc.