Back

Glycolysis inhibition functionally reprograms T follicular helper cells and reverses lupus

Elshikha, A.; Ge, Y.; Choi, S. C.; Park, Y. P.; Padilla, L.; Zhu, Y.; Clapp, W. L.; Sobel, E. S.; Mohamadzadeh, M.; Morel, L.

2024-10-18 immunology
10.1101/2024.10.15.618563 bioRxiv
Show abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease in which the production of pathogenic autoantibodies depends on T follicular helper (TFH) cells. This study was designed to investigate the mechanisms by which inhibition of glycolysis with 2-deoxy-d-glucose (2DG) reduces the expansion of TFH cells and the associated autoantibody production in lupus-prone mice. Integrated cellular, transcriptomic, epigenetic and metabolic analyses showed that 2DG reversed the enhanced cell expansion and effector functions, as well as mitochondrial and lysosomal defects in lupus TFH cells, which include an increased chaperone-mediated autophagy induced by TLR7 activation. Importantly, adoptive transfer of 2DG-reprogrammed TFH cells protected lupus-prone mice from disease progression. Orthologs of genes responsive to 2DG in murine lupus TFH cells were overexpressed in the TFH cells of SLE patients, suggesting a therapeutic potential of targeting glycolysis to eliminate aberrant TFH cells and curb the production of autoantibodies inducing tissue damage.

Matching journals

The top 7 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.