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

 Anomalies of ILCs in NHL and HL.

PopulationNHLHL
NK cellsCD56 bright NK cells showed an increased downregulation of the maturation molecule KLRG1, the activation markers CD38, CD62L, and CD94, and an upregulation of CD73 [120].
CD73 and CD39 expression increased in CD16+ NKs [115].
Type II NKT cells had a suppressive role in the immune response against cancer, while type I NKT cells had a protective role [93].
When joined in an IL-12–IL-2 fusion protein, the IL-2 and IL-12 cytokine domains displayed reciprocal activity to activate T-cells; they also maintained their activity when connected to CD30+ target cells via a fused antibody.
The growth of cancer in mice given saline solution as a control was prevented by a dual cytokine fusion protein. Since the HRS3-IL12-Fc-IL2 fusion protein had no effect on the growth of the C10 hybridoma, the inhibition of cancer growth was target-antigen-specific [136].

ILCs: innate lymphoid cells; NHLs: non-Hodgkin lymphomas; HLs: Hodgkin lymphomas; NK: natural killer; KLRG1: killer cell lectin-like receptor G1. These findings highlight the complex roles of ILCs in lymphomas and suggest promising therapeutic avenues that involve modulating ILC activity to enhance anti-tumor immunity or mitigate tumor-promoting effects.