期刊
CANCER IMMUNOLOGY RESEARCH
卷 1, 期 5, 页码 332-339出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/2326-6066.CIR-13-0084
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资金
- University of Virginia School of Medicine's Cancer Biology Training Grant [USPHS T32 CA009109]
- Geisel School of Medicine at Dartmouth's Immunology Training Grant [USPHS T32 AI007363]
- Joanna M Nicolay Melanoma Research Foundation
- Melanoma Research Alliance
- USPHS [R21 CA103528, R01 CA134799]
T-cell infiltration of melanoma is associated with enhanced clinical efficacy and is a desirable endpoint of immunotherapeutic vaccination. Infiltration is regulated, in part, by chemokine receptors and selectin ligands on the surface of tumor-specific lymphocytes. Therefore, we investigated the expression of two homing molecules, CXC chemokine receptor 3 (CXCR3) and cutaneous lymphocyte antigen (CLA), on vaccine-induced CD8 T cells, in the context of a clinical trial of a melanoma-specific peptide vaccine. Both CXCR3 and CLA have been associated with T-cell infiltration of melanoma. We show that a single subcutaneous/intradermal administration of peptide vaccine in Montanide adjuvant induces tumor-specific CD8 T cells that are predominantly positive for CXCR3, with a subpopulation of CXCR3(+)CLA(+) cells. Addition of granulocyte macrophage colony-stimulating factor (GM-CSF) significantly enhances CXCR3 expression and increases the proportion of CLA-expressing cells. Concurrent with CXCR3 and CLA expression, vaccine-induced CD8 cells express high levels of T-bet, IFN-gamma, and interleukin-12 receptor (IL-12R beta 1). Collectively, these studies show that peptide vaccination in adjuvant induces CD8 T cells with a phenotype that may support infiltration of melanoma. (C) 2013 AACR.
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