Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 200, Issue 1, Pages 115-122Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20040612
Keywords
autoimmunity; antibody secretion; cellular differentiation; immunoglobulin; IRF-4
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Funding
- NIAID NIH HHS [AI01803, AI057471, R01 AI057471] Funding Source: Medline
- NIDDK NIH HHS [DK52574, P30 DK052574] Funding Source: Medline
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B cell terminal differentiation involves development into an antibody-secreting plasma cell, reflecting the concerted activation of proplasma cell transcriptional regulators, such as Blimp-1, IRF-4, and Xbp-1. Here, we show that the microphthalmia-associated transcription factor (MitF) is highly expressed in naive B cells, where it antagonizes the process of terminal differentiation through the repression of IRF-4. Defective Mitf activity results in spontaneous B cell activation, antibody secretion, and autoantibody production. Conversely, ectopic Mitf expression suppresses the expression of IRF-4, the plasma cell marker CD138, and antibody secretion. Thus, Mitf regulates B cell homeostasis by suppressing the antibody-secreting fate.
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