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Myc-Interacting Zinc Finger Protein 1 (Miz-1) Is Essential to Maintain Homeostasis and Immunocompetence of the B Cell Lineage.

Authors
  • Piskor, Eva-Maria1
  • Ross, Julie2
  • Möröy, Tarik2, 3, 4
  • Kosan, Christian1
  • 1 Institute of Biochemistry and Biophysics, Center for Molecular Biomedicine (CMB), Friedrich Schiller University, Hans-Knöll-Str. 2, 07745 Jena, Germany. , (Germany)
  • 2 Hematopoiesis and Cancer Unit, Institut de Recherches Cliniques de Montréal (IRCM), 110 av. Des Pins O, Montréal, QC H2W 1R7, Canada. , (Canada)
  • 3 Département de Microbiologie, Infectiologie et Immunologie, Université de Montréal, 2900, boul. Édouard-Montpetit, Montréal, QC H3T 1J4, Canada. , (Canada)
  • 4 Division of Experimental Medicine, McGill University, 801 Sherbrooke St. W., Montréal, QC H3A 0B8, Canada. , (Canada)
Type
Published Article
Journal
Biology
Publication Date
Mar 24, 2022
Volume
11
Issue
4
Identifiers
DOI: 10.3390/biology11040504
PMID: 35453704
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Aging of the immune system is described as a progressive loss of the ability to respond to immunologic stimuli and is commonly referred to as immunosenescence. B cell immunosenescence is characterized by a decreased differentiation rate in the bone marrow and accumulation of antigen-experienced and age-associated B cells in secondary lymphoid organs (SLOs). A specific deletion of the POZ-domain of the transcription factor Miz-1 in pro-B cells, which is known to be involved in bone marrow hematopoiesis, leads to premature aging of the B cell lineage. In mice, this causes a severe reduction in bone marrow-derived B cells with a drastic decrease from the pre-B cell stage on. Further, mature, naïve cells in SLOs are reduced at an early age, while post-activation-associated subpopulations increase prematurely. We propose that Miz-1 interferes at several key regulatory checkpoints, critical during B cell aging, and counteracts a premature loss of immunocompetence. This enables the use of our mouse model to gain further insights into mechanisms of B cell aging and it can significantly contribute to understand molecular causes of impaired adaptive immune responses to counteract loss of immunocompetence and restore a functional immune response in the elderly.

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