Bryostatin 1-activated T cells can traffic and mediate tumor regression

J Surg Res. 1992 Jun;52(6):543-8. doi: 10.1016/0022-4804(92)90126-k.

Abstract

Adoptive immunotherapy in humans may be limited by the lack of autologous tumor cells to activate and expand tumor-specific T cells. Pharmacologic manipulation of protein kinase C (PKC) and intracellular calcium may substitute for tumor antigen and stimulate T cells for adoptive immunotherapy. In the present study, we evaluated the ability of the PKC activator Bryostatin 1 (B) plus the calcium ionophore ionomycin (I) to activate lymphocytes obtained from popliteal lymph nodes (DLN) draining an MCA-105 footpad tumor. The adoptive transfer of B/I-stimulated DLN cells eradicated MCA-105 pulmonary metastases. These lymphocytes do not require concomitant IL-2 administration to mediate regression of lung metastases. Three days after intrasplenic injection of tumor cells and splenectomy, mice were given iv injections of B/I-stimulated DLN cells. Adoptive immunotherapy with these cells induced regression of established liver metastases. In an intradermal tumor model, the adoptive transfer of B/I-stimulated MCA-105 DLN cells cured mice of MCA-105 intradermal (id) tumors, but did not induce regression of MCA-206 tumors. Mice cured of MCA-105 id tumors were protected against MCA-105, but not MCA-203, tumor challenge in the footpad 7 weeks after adoptive immunotherapy.

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology*
  • Bryostatins
  • Female
  • Immunotherapy, Adoptive
  • Lactones / pharmacology*
  • Liver Neoplasms, Experimental / secondary
  • Lung Neoplasms / secondary
  • Lymphocyte Activation / drug effects*
  • Macrolides
  • Mice
  • Mice, Inbred C57BL
  • Neoplasms, Experimental / immunology
  • Neoplasms, Experimental / therapy*
  • T-Lymphocytes / immunology*

Substances

  • Antineoplastic Agents
  • Bryostatins
  • Lactones
  • Macrolides
  • bryostatin 1