Myeloid-derived suppressor cells (MDSCs) occupy sites of chronic inflammation and suppress CD8+ T cell function. A new study describes the transfer of the metabolite methylglyoxal (MG) to T cells, which mediates this immunosuppressive mechanism.
The immunosuppressive activity of MDSCs is an important yet mysterious aspect of the immune-evasive tumor microenvironment. In this issue of Nature Immunology, Baumann et al. uncover a novel mechanism for the MDSC-dependent metabolic and functional paralysis of CD8+ T cells, which involves the cytosolic transfer of the toxic dicarbonyl-molecule MG to T cells via cell-to-cell transmission.
Nature Immunology 21, 497–498(2020)
