Effects of anti-NKG2A antibody administration on leukemia and normal hematopoietic cells

Ruggeri, Loredana; Urbani, Elena; Pèlegrin, André; Mancusi, Antonella; Tosti, Antonella; Topini, Fabiana; Bléry, Mathieu; Animobono, Lucia; Romagné, François; Wagtmann, Nicolai; Velardi, Andrea

doi:10.3324/haematol.2015.135301

Cited by 136 publications

(108 citation statements)

References 27 publications

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“…Nevertheless, there is ample experimental evidence regarding the specificity of NKG2A and HLA-E binding [45–48]. The inhibitory CD94/NKG2A receptor belongs to the C-type lectin family of proteins [45].…”

Section: Discussionmentioning

confidence: 99%

Tonsillar CD56brightNKG2A+ NK cells restrict primary Epstein-Barr virus infection in B cells via IFN-γ

et al. 2016

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Natural killer (NK) cells constitute the first line of defense against viruses and cancers cells. Epstein–Barr virus (EBV) was the first human virus to be directly implicated in carcinogenesis, and EBV infection is associated with a broad spectrum of B cell lymphomas. How NK cells restrict EBV-associated oncogenesis is not understood. Here, we investigated the efficacies and mechanisms of distinct NK cell subsets from tonsils, the portal of entry of EBV, in limiting EBV infection in naïve, germinal center-associated and memory B cells. We found that CD56bright and NKG2A expression sufficiently characterizes the potent anti-EBV capacity of tonsillar NK cells. We observed restriction of EBV infection in B cells as early as 18 hours after infection. The restriction was most efficient in naïve B cells and germinal center-associated B cells, the B cell subsets that exhibited highest susceptibility to EBV infection in vitro. IFN-γ release by and partially NKp44 engagement of CD56bright and NKG2A positive NK cells mediated the restriction that eventually inhibited B-cell transformation. Thus, harnessing CD56brightNKG2A+ NK cell function might be promising to improve treatment strategies that target EBV-associated B cell lymphomas.

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Section: Discussionmentioning

confidence: 99%

Tonsillar CD56brightNKG2A+ NK cells restrict primary Epstein-Barr virus infection in B cells via IFN-γ

et al. 2016

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“…Lirilumab and monalizumab are two IgG4 mAbs that antagonize KIR2D and NKG2A, respectively. In preclinical mouse models, both mAbs have been shown to enhance NK cell responses against HLA‐I proficient tumour cell lines with limited side effects . Particularly, NKG2A targeting efficiently synergizes with PD‐1 blockade unleashing the effector functions of both NK and CD8 + T cells, a phenomenon probably due to the high and wide expression of HLA‐E on tumour cells .…”

Section: Natural Killer Cells and Melanoma Immunotherapymentioning

confidence: 99%

New avenues for melanoma immunotherapy: Natural Killer cells?

et al. 2020

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Human solid malignant tumours may be particularly resistant to conventional therapies. Among solid tumours, immunological features of cutaneous melanoma have been well characterized in the past and today melanoma patients are routinely treated with the anti‐immune checkpoints immunotherapy that has completely changed metastatic melanoma treatment and prognosis. Two cytotoxic cell populations may lead to the physical elimination of tumour cell targets: cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. Tumour recognition by CTLs depends on major histocompatibility complex (MHC) class I molecules, while NK cells recognize tumours expressing low or null levels of MHC class I molecules. Despite this well‐established complementarity, NK cells are still left behind in the optimization of innovative immunotherapy approaches. NK cells are members of innate lymphoid cells (ILCs) that play a critical role in early host defence against invading pathogens and transformed cells. Recent findings suggest that NK cell frequencies directly correlate with the overall survival of ipilimumab‐treated melanoma patients. Furthermore, in vitro and in vivo evidences indicate that NK cells can selectively kill cancer stem cells, reducing tumour size and delaying metastatic progression. The aim of this review is to provide a survey of the evidences indicating NK cells as an excellent candidate to complement the newest solid tumour immunotherapy approaches.

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“…Antibody-activated NK cells also effectively eliminated patient AML cells in vivo [36]. Anti-human NKG2A mAb have also been explored as a means of selectively differentiating and optimizing NK cells [37]. NKG2A…”

Section: Alternative Sources Of Nk Cellsmentioning

confidence: 99%

Advances in Immunotherapy for Acute Myeloid Leukemia

2018

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Evasion of the host immune system is a key mechanism to promote malignant progression. Therapeutically targeting immune pathways has radically changed the treatment paradigm for solid and lymphoid tumors but has yet to be approved for myeloid malignancies. Here, we summarize the most recent advances in immunotherapy for acute myeloid leukemia. Topics reviewed here include adoptive cellular approaches (chimeric antigen receptor-T cells, natural killer and other immune cells), checkpoint inhibitors (anti-PD-1/PD-L1, anti-CTLA-4 and TIM-3) and vaccines (WT-1, HLA-A2 and hTERT). Emphasis is placed on agents with clear evidence of tumor-specific immune responses and/or clinical activity in early-phase trials. Despite concerns regarding heterogeneous antigen expression and cytokine release syndrome, immunotherapy remains a highly promising strategy for acute myeloid leukemia, particularly transplant-ineligible patients and minimal residual disease states.

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Effects of anti-NKG2A antibody administration on leukemia and normal hematopoietic cells

Cited by 136 publications

References 27 publications

Tonsillar CD56brightNKG2A+ NK cells restrict primary Epstein-Barr virus infection in B cells via IFN-γ

Tonsillar CD56brightNKG2A+ NK cells restrict primary Epstein-Barr virus infection in B cells via IFN-γ

New avenues for melanoma immunotherapy: Natural Killer cells?

Advances in Immunotherapy for Acute Myeloid Leukemia

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