Insights into the mechanism of anti-tumor immunity in mice vaccinated with the human HER2/neu extracellular domain plus anti-HER2/neu IgG3-(IL-2) or anti-HER2/neu IgG3-(GM-CSF) fusion protein.

Abstract

In the present study, we demonstrate that a physical association between the extracellular domain of human HER2/neu receptor (ECDHER2) plus anti-HER2/neu IgG3-(IL-2) or anti-HER2/neu IgG3-(GM-CSF) was required to elicit the most effective anti-tumor immune response against a syngeneic tumor expressing rat HER2/neu. Immune effectors including CD4+, CD8+, and NK cells contributed to protection against tumor growth. Vaccinated B-cell deficient mice did not elicit tumor protection, suggesting a critical role for B-cells in a protective immune response. These results provide insights into the mechanisms responsible for the protective tumor immunity elicited when antibody-(IL-2 or GM-CSF) are used as enhancers of vaccines targeting tumor antigens.

• Authors: Jay S Dela Cruz, Sherie L Morrison, Manuel L Penichet
• Journal: Vaccine (Vaccine) Vol. 23 Issue 39 Pg. 4793-803 (Sep 15 2005) ISSN: 0264-410X [Print] Netherlands
• PMID: 15967544 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Cancer Vaccines
• Immunoglobulin G
• Recombinant Fusion Proteins
• Vaccines, Synthetic
• Granulocyte-Macrophage Colony-Stimulating Factor
• Receptor, ErbB-2

Topics

• Animals
• B-Lymphocytes (immunology)
• CD4-Positive T-Lymphocytes (immunology)
• CD8-Positive T-Lymphocytes (immunology)
• Cancer Vaccines (immunology)
• Female
• Granulocyte-Macrophage Colony-Stimulating Factor (immunology)
• Humans
• Immunoglobulin G (immunology)
• Killer Cells, Natural (immunology)
• Mice
• Mice, Inbred BALB C
• Receptor, ErbB-2 (immunology)
• Recombinant Fusion Proteins (immunology)
• Vaccination
• Vaccines, Synthetic (immunology)