Acute myeloid leukemia cells fail to activate native human dendritic cells: a potential mechanism of immune evasion

Wehner, Rebekka; Schumacher, Petra B.; Bornhäuser, Martin; Ehninger, Gerhard; Schäkel, Knut; Bachmann, Michael; Schmitz, Marc

doi:10.1038/leu.2010.189

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Indirect Effects Of Type I Ifn Through Immune Activation1

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2011

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“…NK cells are increasingly being recognized as essential components of the antileukemic immune response. 35,36 Although these cells are able to recognize and eliminate AML blasts and even leukemic stem cells, 37 they often fail to do so effectively. [38][39][40][41][42][43][44][45][46] As summarized in Table 1, several mechanisms may account for the defective cytotoxic effector function of NK cells in AML.…”

Section: Indirect Effects Of Type I Ifn Through Immune Activationmentioning

confidence: 99%

Interferon-α in acute myeloid leukemia: an old drug revisited

et al. 2011

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Interferon-a (IFN-a), a type I IFN, is a well-known antitumoral agent. The investigation of its clinical properties in acute myeloid leukemia (AML) has been prompted by its pleiotropic antiproliferative and immune effects. So far, integration of IFN-a in the therapeutic arsenal against AML has been modest in view of the divergent results of clinical trials. Recent insights into the key pharmacokinetic determinants of the clinical efficacy of IFN along with advances in its pharmaceutical formulation, have sparked renewed interest in its use. This paper reviews the possible applicability of IFN-a in the treatment of AML and provides a rational basis to re-explore its efficacy in clinical trials.

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