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Effect of B7.1 costimulation on T-cell based immunity against TAP-negative cancer can be facilitated by TAP1

Xiao-Lin Li1, Yong-Yu Liu, David Knight

  • 1Department of Cellular Biology and Anatomy, Gene Therapy Program, Louisiana State University Health Sciences Center, Shreveport, Louisiana, United States of America.

Plos One
|July 25, 2009
PubMed

Insights

Introducing the B7.1 gene into tumors deficient in transporter associated with antigen processing (TAP) enhances immune response. Co-expression of B7.1 and TAP1 genes is crucial for effective anti-tumor immunity and reduced tumorigenicity in TAP-negative cancers.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Tumors lacking the transporter associated with antigen processing (TAP) typically evade T-cell immunity and resist T-cell-mediated killing.
  • The B7.1 co-stimulatory molecule plays a role in immune responses.
  • Transporter associated with antigen processing (TAP) is essential for presenting antigens to T cells.

Purpose of the Study:

  • To investigate the potential of introducing the B7.1 gene into TAP-deficient (TAP(-)) and TAP1-transfected (TAP1(+)) murine lung carcinoma cells to enhance anti-tumor immunity.
  • To evaluate the combined effect of B7.1 and TAP1 gene expression on protective anti-tumor responses.

Main Methods:

  • Transfection of CMT.64 murine lung carcinoma cells with B7.1 and/or TAP1 genes.
  • Immunization of mice with gamma-irradiated B7.1-expressing TAP(-) or TAP1(+) CMT.64 cells at varying doses.
  • Assessment of T-cell mediated immunity through CD8 and CD4 cell depletion studies.
  • Infection of tumor cells with vaccinia viruses carrying B7.1 and/or TAP1 genes for immunization.
  • Evaluation of tumorigenicity following inoculation with gene-transfected live tumor cells.

Main Results:

  • Introduction of the B7.1 gene into TAP(-) or TAP1(+) CMT.64 cells augmented the capacity to induce protective immunity against wild-type tumor cells.
  • Immunization with B7.1-expressing TAP1(+) cells was more effective than B7.1-expressing TAP(-) cells in inducing tumor rejection, with dose dependency observed.
  • Protective immunity was T-cell dependent, as evidenced by reduced anti-tumor responses in CD8 or CD4 depleted mice.
  • Co-expression of both B7.1 and TAP1 in virally infected tumor cells was necessary to induce protective immunity against CMT.64 cells.
  • Only B7.1 and TAP1 co-expressing tumor cells significantly reduced tumorigenicity when inoculated as live cells.

Conclusions:

  • B7.1-mediated anti-tumor immunity against TAP-deficient cancers is facilitated by TAP1 expression.
  • Combined therapeutic strategies involving B7.1 and TAP1 warrant consideration for future cancer treatment, particularly for TAP-deficient tumors.

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