Publication highlights

Researchers at the Crick and Australian National University have shown how two proteins, TCF1 and LEF1, previously only studied in T cells, enable B-1 cells (a type of innate B cell which remains uncharacterised in humans) to apply the brakes on inflammation in mice and used this information to identify signs of B-1 activity in humans. They found that removing TCF1 and LEF1 in adult mice led to the production of a smaller number of dysfunctional B-1a cells that failed to restrain an immune assault on the brain resembling multiple sclerosis. Cells without TCF1 and LEF1 also produced significantly less of an anti-inflammatory compound, IL-10. Finally, the team analysed pleural fluid from people with pleural infections, finding an abundance of B-1-like cells which expressed both genes, as did malignant B cells in people with chronic lymphocytic leukaemia. They also conclude that TCF1 and LEF1 could be harnessed to increase the effectiveness of other immune cells.

Researchers at the Francis Crick Institute, the National Cancer Institute (NCI) of the U.S. National Institutes of Health (NIH) and Aalborg University in Denmark, have found that mice given a diet rich in vitamin D had better immune resistance to experimentally transplanted cancers and improved responses to immunotherapy treatment. They found that vitamin D acts on epithelial cells in the intestine, which in turn increase the amount of Bacteroides fragilis bacteria. Mice on a normal diet given the bacteria were also better able to resist tumour growth, but not when the mice were placed on a vitamin D-deficient diet. Although Bacteroides fragilis is also found in the microbiome in humans, more research is needed to understand whether vitamin D helps provide some immune resistance to cancer through the same mechanism.