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FIP200 regulates plasma B cell differentiation via mitochondrial and heme homeostasis

Year: 2025
Type: article
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.
DOI: 10.1084/jem.20250535
Authors: 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
Institutions: Ragon Institute of MGH, MIT and Harvard, Massachusetts Institute of Technology, Newcastle University, University of Dundee, MRC Protein Phosphorylation and Ubiquitylation Unit, Harvard University
Language: English
Subfield: Epidemiology
Field: Medicine
Open Access status: hybrid
OpenAlex ID: W4417434957
FWCI: 0.603
Cites: 77
Cited by: 1
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