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. 2012 Mar 1;1(2):211–213. doi: 10.4161/onci.1.2.18100

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Copyright © 2012 Landes Bioscience

This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

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Figure 1. — The potential role of CLIP in AML immunopathogenesis and immunotherapy. Situations before and after immunotherapy in patients with AML are proposed: (A) Tumor immunity in untreated CLIP^- AML; LAA-specific T cell priming and recognition are optimal due to enhanced endogenous LAA presentation by leukemic cells. (B) Tumor immune escape in untreated CLIP⁺ AML; leukemia-specific T cell priming as well as recognition are hampered because of inhibition of DC function and low immunogenicity by CLIP⁺ leukemic cells. (C) Tumor immune escape in treated CLIP⁺ AML; although priming of leukemia-specific T cells is resolved by DC vaccination or T cell transfer, leukemic cells still escape their recognition by expressing CLIP. (D) Tumor immunity in treated CLIP⁺ AML; by using DC vaccination or T cell transfer in combination with in vivo immunomodulatory drugs, both T cell priming and recognition are targeted, which might induce a potent immune response against leukemic cells.