Costimulation by CD48 and B7-1 induces immunity against poorly immunogenic tumors

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Y Li1, K E Hellstrom, S A Newby

  • 1Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, Washington 98121, USA.

The Journal of Experimental Medicine
|February 1, 1996
PubMed

Insights

Enhancing tumor immunogenicity for cancer therapy: Combining B7-1 and CD48 gene transfection in mouse models successfully generated anti-tumor immune responses, offering a potential strategy for treating poorly immunogenic tumors.

Area of Science:

  • Immunology
  • Cancer Biology
  • Molecular Genetics

Background:

  • Genetic modification of mouse tumors with B7-1 or B7-2 molecules enhances immunogenicity.
  • Poorly immunogenic tumors often fail to elicit effective immune responses even after B7 gene transfection.

Purpose of the Study:

  • To investigate if co-expression of B7-1 and CD48 can render poorly immunogenic mouse tumors (Ag104A sarcoma, K1735-M2 melanoma) immunogenic.
  • To evaluate the potential of this combined gene therapy approach for cancer immunotherapy.

Main Methods:

  • Transfection of Ag104A sarcoma and K1735-M2 melanoma cells with genes encoding murine B7-1 and CD48.
  • Generation of tumor-specific CD8+ cytotoxic T lymphocytes (CTLs).
  • Assessment of CTL efficacy in adoptive immunotherapy against wild-type Ag104A sarcoma-induced metastasis.

Main Results:

  • Co-transfection with B7-1 and CD48 genes successfully induced immunogenicity in previously poorly immunogenic tumors.
  • Tumor-specific CD8+ CTLs were readily generated.
  • Adoptive immunotherapy using these CTLs was effective against metastasis.

Conclusions:

  • Combined B7-1 and CD48 gene transfer is a viable strategy to enhance the immunogenicity of poorly immunogenic tumors.
  • This approach holds promise for developing novel immunotherapies for various cancers, potentially including human tumors.

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