Cancer Immunology, Immunotherapy

, Volume 24, Issue 1, pp 8–12 | Cite as

The role of tumor-specific Lyt-1+2− T cells in eradicating tumor cells in vivo

II. Lyt-1+2− T cells have potential to reject antigenically irrelevant (bystander) tumor cells on activation with the specific target tumor cells
  • Takayuki Yoshioka
  • Hiromi Fujiwara
  • Yasuyuki Takai
  • Masato Ogata
  • Jun Shimizu
  • Toshiyuki Hamaoka
Original Articles
Received:
Accepted:

Summary

The present study investigates some of mechanisms for tumor-specific Lyt-1+2− T cell-mediated tumor cell eradication in vivo through analyses of tumor specificity in the afferent tumor recognition and efferent rejection phases. When C3H/He mice which had acquired immunity against syngeneic MH134 hepatoma were challenged with other syngeneic X5563 plasmacytoma cells, these mice failed to exhibit any inhibitory effect on the growth of X5563 tumor cells. However, the inoculation of X5563 tumor cells into the MH134-immune C3H/He mice together with the MH134 tumor cells resulted in appreciable growth inhibition of antigenically distinct (bystander) X5563 tumor cells. Although the growth of X5563 cells was inhibited in an antigen-nonspecific way in mice immunized to antigenically unrelated tumor cells (bystander effect), the activation of Lyt-1+2− T cells leading to this effect was strictly antigen-specific. Such a bystander growth inhibition also required the admixed inoculation of the bystander (X5563) and specific target (MH134) tumor cells into a single site in mice immunized against the relevant MH134 tumor cells. Furthermore, the results demonstrated that Lyt-1+2− T cells specific to MH134 tumor cells were responsible for mediating the growth inhibition of antigenically irrelevant (bystander) and relevant tumor cells. These results are discussed in the context of cellular and molecular mechanisms involved in the Lyt-1+2− T cell-initiated bystander phenomenon.

Keywords

Tumor Cell Growth Inhibition Tumor Specificity Bystander Effect Plasmacytoma 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Copyright information

© Springer-Verlag 1987

Authors and Affiliations

  • Takayuki Yoshioka
    • 1
  • Hiromi Fujiwara
    • 1
  • Yasuyuki Takai
    • 1
  • Masato Ogata
    • 1
  • Jun Shimizu
    • 1
  • Toshiyuki Hamaoka
    • 1
  1. 1.From the Department of Oncogenesis, Institute for Cancer ResearchOsaka University Medical SchoolOsakaJapan

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