Epitope spreading upon P815 tumor rejection triggered by vaccination with the single class I MHC-restricted peptide P1A
Epitope spreading upon P815 tumor rejection triggered by vaccination with the single class I MHC-restricted peptide P1A
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DOI:
10.1093/intimm/13.5.625
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发表时间:
2001-05-01
影响因子:
4.4
通讯作者:
Gajewski, TF
中科院分区:
文献类型:
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作者:
Markiewicz, MA;Fallarino, F;Gajewski, TF
Epitope spreading has been best characterized as an exacerbating factor in CD4(+) T cell-dependent autoimmune disease models and is believed to occur via presentation of antigens liberated by tissue destruction initiated by CD4+ T cells specific for a primary epitope, The growing evidence that exogenous antigens can also be processed and presented by class I MHC molecules has suggested that epitope spreading could occur for CD8(+) cytotoxic T lymphocyte (CTL) responses as well, In the context of anti-tumor immunity, expansion of a CTL response to include secondary epitopes could improve the efficacy of therapeutic vaccines, To determine directly whether epitope spreading can occur during an anti-tumor immune response, two defined class I MHC-binding peptides in the P815 tumor model were utilized. We observed that immunization against the single tumor peptide, P1A, followed by rejection of a P1A(+) tumor, subsequently yielded CTL activity and tumor protection against a P1A(-) tumor variant, P1A immunized mice that subsequently rejected tumor challenge developed CTL against a second defined epitope, P1E. These results indicate that, as for class II-restricted peptides in autoimmune disease, epitope spreading can occur for class II-restricted peptides during tumor rejection. A broadened CT response may help eliminate outgrowth of antigen-negative tumor variants.