Back

Diacylglycerol kinase zeta dictates CD40-mediated immune synapse formation, mTORC1 signaling and plasma cell fate in B lymphocytes

Fernandez-Barrecheguren, A.; Fernandez-Rego, A.; Fuentes-Cantos, L.; Pons, T.; Estrada, B. S.; Iborra-Pernichi, M.; Ebrahimi, T.; Sagrera-Aparisi, A.; Cogliati, S.; Martinez-Martin, N.; Jimenez-Saiz, R.; Carrasco, Y. R.

2025-01-14 immunology
10.1101/2025.01.11.632541 bioRxiv
Show abstract

To mount a robust T-dependent immune response, antigen-specific B lymphocytes require CD40 stimulation through immune synapse formation with CD4+ T follicular helper cells. CD40 triggers the activation of mammalian target of rapamycin complex-1 (mTORC1) and remodels the mitochondria to meet increased bioenergetic and anabolic demands. We show that diacylglycerol-kinase-{zeta} (DGK{zeta}) has a crucial role in activating the mTORC1 pathway and remodeling mitochondria downstream of CD40 signaling in B cells. DGK{zeta} governs organelle translocation to the CD40-mediated immune synapse and the recruitment of mTORC1 to lysosomes. DGK{zeta}-/- B cells exhibited impaired mitochondria function, protein biosynthesis, metabolite transporter expression and cell cycle progression, accompanied by dysregulation of the transcriptional network governing B cell fate. These defects lead to a blockage in the progression of the germinal center response and plasma cell differentiation in vivo. Our findings establish DGK{zeta} as a key mediator of CD40 functions in the B cell response.

Published in Science Signaling · training set

Matching journals

The top 5 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.