FIP200 regulates plasma B cell differentiation via mitochondrial and heme homeostasis
Name
jem_20250535.pdf
Description
Published version
Size
7.92 MB
Format
Adobe PDF
Checksum (MD5)
54204ba12301c09444996f24ee260e57
Author(s)
Xu, Liling
Bottermann, Maria
Villavicencio, Paula M
Warner, John
Weldon, Stephanie R
Xie, Zhenfei
Filby, Andrew
Liu, Xiaotie
Ganley, Ian G
Ringel, Alison E
Date Issued
March 2, 2026
Journal
Journal of Experimental Medicine
Publisher
Rockefeller University Press
Citation
Liling Xu, Maria Bottermann, Paula M. Villavicencio, John Warner, Stephanie R. Weldon, Zhenfei Xie, Andrew Filby, Xiaotie Liu, Ian G. Ganley, Alison E. Ringel, Usha Nair, Facundo D. Batista; FIP200 regulates plasma B cell differentiation via mitochondrial and heme homeostasis. J Exp Med 2 March 2026; 223 (3): e20250535.
Version
Final published version
Abstract
Little is known about the role of autophagy in the human humoral immune system. Here, we found that in B cells, genetic ablation of FIP200, a mammalian metabolic sensor that regulates autophagy in response to a range of stimuli, led to diminished humoral immune responses in mice. FIP200-deficient B cells displayed decreased differentiation into plasma cells, as well as mitochondrial dysfunction, alterations in heme biosynthesis, and significant cell death. Notably, the addition of heme was sufficient to rescue plasma cell differentiation of FIP200-deficient B cells. Thus, FIP200 determines B cell fates by controlling mitophagy and metabolic reprogramming.
Terms of Use
Creative Commons Attribution
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1084/jem.20250535
