TY - JOUR
T1 - Effects of murine tumor class i major histocompatibility complex expression on antitumor activity of tumor-infiltrating lymphocytes
AU - Weber, Jeffrey S.
AU - Rosenberg, Steven A.
PY - 1990/5/2
Y1 - 1990/5/2
N2 - Tumor-infiltrating lymphocytes (TILs) are T cells that can be grown from enzyme-digested murine or human tumors. When adoptively transferred to tumor-bearing hosts concurrent with the administration of recombinant interleukin-2 (rIL-2), TILs can mediate significant regression of tumor. To examine whether expression of class I major histocompatibility complex on tumor cells influenced the generation and antitumor activity of TILs, we used clones of murine B16BL6 melanoma either transfected with or lacking the class I gene Kb to generate TILs at a high dose (1, 000 U/mL) or at a low dose (20 U/mL) of human rIL-2. TILs grew from both tumors in high-dose rIL-2, but they grew from the class I-expressing tumor only in low-dose rIL-2. TILs from the class I-deficient tumor did not lyse any target tested in vitro, nor did they demonstrate any therapeutic effect in vivo on established tumors that lacked or expressed class I. In contrast, TILs from the class I-expressing tumor specifically lysed the tumor of origin in vitro and caused it to regress in vivo. Further, these TILs demonstrated activity in vitro against the non-class I-expressing melanoma treated with the combination of murine recombinant interferony and human recombinant tumor necrosis factor α in vivo, when administered with recombinant interferon γ and recombinant tumor necrosis factor a, TILs from the class I-expressing tumor mediated regression of non-class I-expressing pulmonary metastases, presumably by augmenting class I expression. [J Natl Cancer Inst 82: 755-761, 1990]
AB - Tumor-infiltrating lymphocytes (TILs) are T cells that can be grown from enzyme-digested murine or human tumors. When adoptively transferred to tumor-bearing hosts concurrent with the administration of recombinant interleukin-2 (rIL-2), TILs can mediate significant regression of tumor. To examine whether expression of class I major histocompatibility complex on tumor cells influenced the generation and antitumor activity of TILs, we used clones of murine B16BL6 melanoma either transfected with or lacking the class I gene Kb to generate TILs at a high dose (1, 000 U/mL) or at a low dose (20 U/mL) of human rIL-2. TILs grew from both tumors in high-dose rIL-2, but they grew from the class I-expressing tumor only in low-dose rIL-2. TILs from the class I-deficient tumor did not lyse any target tested in vitro, nor did they demonstrate any therapeutic effect in vivo on established tumors that lacked or expressed class I. In contrast, TILs from the class I-expressing tumor specifically lysed the tumor of origin in vitro and caused it to regress in vivo. Further, these TILs demonstrated activity in vitro against the non-class I-expressing melanoma treated with the combination of murine recombinant interferony and human recombinant tumor necrosis factor α in vivo, when administered with recombinant interferon γ and recombinant tumor necrosis factor a, TILs from the class I-expressing tumor mediated regression of non-class I-expressing pulmonary metastases, presumably by augmenting class I expression. [J Natl Cancer Inst 82: 755-761, 1990]
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U2 - 10.1093/jnci/82.9.755
DO - 10.1093/jnci/82.9.755
M3 - Article
C2 - 2109092
AN - SCOPUS:0025332036
SN - 0027-8874
VL - 82
SP - 755
EP - 761
JO - Journal of the National Cancer Institute
JF - Journal of the National Cancer Institute
IS - 9
ER -