Abstract
BackgroundDepletion of CD25+ Tregs improves anti-tumor immunity in preclinical models. Denileukin diftitox is a recombinant fusion protein of human IL-2 and diptheria toxin fragment that also can kill CD25+ T...
Highlights
Depletion of CD25+ regulatory T cell (Treg) improves anti-tumor immunity in preclinical models
Immune monitoring suggested the development of modest vaccine-specific CD8+ T cell responses in the control group, immunization efficacy was reduced in the denileukin diftitox group
Our results indicate that denileukin diftitox did not effectively deplete Tregs, augment T cell responses, or improve clinical activity in melanoma
Summary
Depletion of CD25+ Tregs improves anti-tumor immunity in preclinical models. Denileukin diftitox is a recombinant fusion protein of human IL-2 and diptheria toxin fragment that can kill CD25+ T cells. The presence of antigens expressed preferentially on tumor cells has suggested tumor-specific vaccination as an immunotherapeutic approach for the treatment of cancer. Vaccines against cancer antigens including Melan-A, gp100, MAGE, and NA17 have been associated with specific T cell immunity and occasional clinical responses [1, 2]. Immunologic correlates of patient response to peptide vaccines are incompletely understood, with some subjects manifesting increased peptide-specific T cell responses as detected in the peripheral blood but no regression of tumor. This general observation has suggested that mechanisms downstream from initial T cell priming may limit the effector phase of the anti-tumor immune response, blunting therapeutic efficacy. Subjects with cancer have been described to have increased Treg cells in both circulation and in the tumor microenvironment [6] with both of these associating with poor prognosis in some studies [7]
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