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Immune evasion is a strategy used by pathogenic organisms and tumours to evade a host's immune response to maximize their probability of being transmitted to a fresh host or to continue growing, respectively.
Most tumours are poorly infiltrated by T cells. Here the authors show that galectin-3 secreted by tumours binds both glycosylated IFNγ and glycoproteins of the tumour extracellular matrix, thus avoiding IFNγ diffusion and the formation of an IFNγ-induced chemokine gradient required for T cell infiltration.
Group 2 innate lymphoid cells (ILC2s) modulate inflammatory and allergic responses, but their function in cancer immunity is still unclear. Here the authors show that, in acute promyelocytic leukaemia, tumour-activated ILC2s secrete IL-13 to induce myeloid-derived suppressor cells and support tumour growth.
A recent article published in Nature describes a novel genetic mechanism of immune evasion in a number of cancers that is caused by structural variants (SVs) disrupting the 3′ regulatory region of programmed cell death ligand 1 (PDL1).