HLA Class I antigens on normal and leukemic cells (quantitative analysis)

Urlacher, A.; Falkenrodt, A.; Tongio, M. M.; Mayer, S.

doi:10.1111/j.1399-0039.1987.tb01583.x

Cited by 9 publications

(1 citation statement)

References 25 publications

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“…Decreased expression of HLA class I molecules is a way for tumor cells to escape specific T-cell surveillance [35, 36]. Interestingly, the downregulation of HLA class I may allow NK cell targeting of tumor cells.…”

Section: Tumor Escape From Nk Cell Surveillance: Role Of Nk Cellsmentioning

confidence: 99%

Hematological Malignancies Escape from NK Cell Innate Immune Surveillance: Mechanisms and Therapeutic Implications

Farnault

Sanchez

Baier

et al. 2012

Clinical and Developmental Immunology

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Hematological malignancies treatment improved over the last years resulting in increased achievement of complete or partial remission, but unfortunately high relapse rates are still observed. Therefore, sustainment of long-term remission is crucial. Immune system has a key role in tumor surveillance. Natural killer (NK) cells, at the frontier of innate and adaptive immune system, have a central role in tumor cells surveillance as demonstrated in the setting of allogenic stem cell transplantation. Nevertheless, tumor cells develop various mechanisms to escape from NK cells innate immune pressure. Abnormal NK cytolytic functions have been described in nearly all hematological malignancies. We present here various mechanisms involved in the escape of hematological malignancies from NK cells surveillance: NK cells quantitative deficiency and NK cell qualitative deficiency by increased inhibition signaling or decreased activating stimuli. A challenge of immunotherapy is to restore an efficient antitumor response. A combination of classical therapy plus immune modulation strategies will soon become a standard of care for hematological malignancies.

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Section: Tumor Escape From Nk Cell Surveillance: Role Of Nk Cellsmentioning

confidence: 99%

Hematological Malignancies Escape from NK Cell Innate Immune Surveillance: Mechanisms and Therapeutic Implications

Farnault

Sanchez

Baier

et al. 2012

Clinical and Developmental Immunology

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Graft Versus Leukemia in Humans

Butturini¹,

Gale²

1995

Cancer Treatment and Research

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Natural killer cells in acute myeloid leukemia patients: from phenotype to transcriptomic analysis

Venton¹,

Labiad²,

Colle³

et al. 2016

Immunol Res

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Chemotherapies allow complete remission in more than 50 % of patients with acute myeloid leukemia (AML), however, with frequent relapse. This suggests that residual leukemic cells may escape to chemotherapy and immune system. Natural killer (NK) cells from AML patients (AML-NK) have a weaker natural cytotoxicity-activating receptors (NCRs) expression than NK cells from healthy donors (HD-NK). Coding genes for NCR1/NKp46, NCR2/NKp44 and NCR3/NKp30 are located at different loci on two different chromosomes; however, their expression is tightly coordinated. Most NK cells express either high (NCR) or low levels (NCR) of all three NCRs. This suggests the existence of negative/positive regulation factor(s) common to the three receptors. In order to find transcription factor(s) or pathway(s) involved in NCRs co-regulation, this study compared the transcriptomic signature of HD-NK and AML-NK cells, before and after in vitro NK cells culture. Microarrays analysis revealed a specific NK cells transcriptomic signature in patients with AML. However, in vitro NK cells expansion erased this signature and up-regulated expression of central molecules of NK functions, such as NCR, NKG2D and also ETS-1, regardless of their origin, i.e., AML-NK vs HD-NK. ETS-1 transcription factor was shown to bind to a specific and common region in the NCRs promoters, thus appearing as a good candidate to explain the coordinated regulation of three NCRs. Such results are encouraging regarding in vitro AML-NK cytotoxicity restoration and provide a new conceptual support for innovative cellular therapy based on in vitro NK cells expansion before their reinfusion in AML patients.

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HLA Class I antigens on normal and leukemic cells (quantitative analysis)

Cited by 9 publications

References 25 publications

Hematological Malignancies Escape from NK Cell Innate Immune Surveillance: Mechanisms and Therapeutic Implications

Hematological Malignancies Escape from NK Cell Innate Immune Surveillance: Mechanisms and Therapeutic Implications

Graft Versus Leukemia in Humans

Natural killer cells in acute myeloid leukemia patients: from phenotype to transcriptomic analysis

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