From:  Phenotypic and functional alterations of innate lymphoid cells in hematological malignancies: potential clinical application

 Anomalies of innate lymphoid cell populations in AML.

PopulationFindings in AML
NKCD57+ KIR+ NK cells are elevated in a subset of AML patients [29].
NKThe inhibition of AHR increases the cytotoxic activity of NK cells on AML blasts and returns normal NK maturation.
NKA less mature peripheral NK cell phenotype characterized by the absence of CD57 and KIR is associated with a reduced overall survival rate [27].
NKIFN-γ secretion is reduced, and NK cytotoxic activity is compromised in AML patients with CD200 HI.
NKA lower level of NK cell function in AML patients is linked to decreased expression of factors that activate the receptors NKp30 and NKp46 and increased production of those that block the receptor NKG2A [31–34].
NKThere have been no observed changes in overall survival in relation to the CMV+ serum status, which is linked to enhanced memory-like NK cell production and extended relapse-free life.
ILC1In AML patients, we have an enrichment and reduced function of null-deficient ILC1 [45], with reduced cytotoxic capabilities [59], and a lower incidence of GVHD [56].
ILC2It was observed that a Treg expansion and HSPC proliferation [51] increased IL-13 secretion [52] and a lower incidence of GVHD [56].
ILC3We have a reduction in spontaneous natural cytotoxic receptor-positive (NCR+) ILC360 normal rates are associated with a favorable prognosis [45] and lower incidence of GVHD [56].
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AML: acute myeloid leukemia; AHR: aryl hydrocarbon receptor; KIR: killer cell immunoglobulin-like receptor; IFN-γ: interferon-gamma; NKp30: natural killer cell protein 30; NKp46: natural killer cell protein 46; CMV: cytomegalovirus; GVHD: graft-versus-host disease; Treg: regulatory T cell; HSPC: hematopoietic stem and progenitor cell.