ABCs begin with ZEB2.
Age‐associated B cells
autoimmune disease
memory B lymphocytes
microbial infection
Journal
Immunology and cell biology
ISSN: 1440-1711
Titre abrégé: Immunol Cell Biol
Pays: United States
ID NLM: 8706300
Informations de publication
Date de publication:
25 Mar 2024
25 Mar 2024
Historique:
medline:
25
3
2024
pubmed:
25
3
2024
entrez:
25
3
2024
Statut:
aheadofprint
Résumé
Age-associated B cells (ABCs) are a stable subset of memory B lymphocytes that develop during microbial infections and in autoimmune diseases. Despite growing appreciation of their phenotypic and functional characteristics, the transcriptional networks involved in ABC fate commitment and maintenance have remained elusive. In their recent publication, Dai et al. tackle this problem, leveraging both mouse models and human diseases to reveal zinc finger E-box-binding homeobox 2 (ZEB2) as a key transcriptional regulator of ABC lineage specification. In aggregate, their results show that ZEB2, a member of the zinc finger E homeobox binding family, promotes ABC differentiation by repressing alternative differentiative fates and targeting genes important for ABC character and function. Moreover, their results strengthen the case for causal links between ABC fate and function in autoimmune pathologies.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2024 the Australian and New Zealand Society for Immunology, Inc.
Références
Dai D, Gu S, Han X, et al. The transcription factor ZEB2 drives the formation of age‐associated B cells. Science 2024; 383: 413–421.
Phalke S, Rivera‐Correa J, Jenkins D, Flores Castro D, Giannopoulou E, Pernis AB. Molecular mechanisms controlling age‐associated B cells in autoimmunity. Immunol Rev 2022; 307: 79–100.
Cancro MP, Age‐Associated B. Cells. Annu Rev Immunol 2020; 38: 315–340.
Wang S, Wang J, Kumar V, et al. IL‐21 drives expansion and plasma cell differentiation of autoreactive CD11chiT‐bet+ B cells in SLE. Nat Commun 2018; 9: 1758.
Holla P, Dizon B, Ambegaonkar AA, et al. Shared transcriptional profiles of atypical B cells suggest common drivers of expansion and function in malaria, HIV, and autoimmunity. Sci Adv 2021; 7: eabg8384.
Jenks SA, Cashman KS, Woodruff MC, Lee FE, Sanz I. Extrafollicular responses in humans and SLE. Immunol Rev 2019; 288: 136–148.
Winslow GM, Papillion AM, Kenderes KJ, Levack RC. CD11c+ T‐bet+ memory B cells: immune maintenance during chronic infection and inflammation? Cell Immunol 2017; 321: 8–17.
Rubtsova K, Rubtsov AV, Cancro MP, Marrack P. Age‐Associated B cells: a T‐bet‐dependent effector with roles in protective and pathogenic immunity. J Immunol 2015; 195: 1933–1937.
Naradikian MS, Myles A, Beiting DP, et al. Cutting edge: IL‐4, IL‐21, and IFN‐gamma interact to govern T‐bet and CD11c expression in TLR‐activated B cells. J Immunol 2016; 197: 1023–1028.
Hagglof T, Vanz C, Kumagai A, et al. T‐bet+ B cells accumulate in adipose tissue and exacerbate metabolic disorder during obesity. Cell Metab 2022; 34: 1121–1136.e6.