한빛사논문
- 조회344
Sunkyung Kim 1, Jing Chen 1, Feiya Ou 1, Tian-Tian Liu 1, Suin Jo 1, William E Gillanders 1, Theresa L Murphy 1, Kenneth M Murphy 1 *
1Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO.
*Corresponding author: correspondence to Kenneth M Murphy
Abstract
Monocytes comprise two major subsets, Ly6Chi classical monocytes and Ly6Clo nonclassical monocytes. Notch2 signaling in Ly6Chi monocytes triggers transition to Ly6C lo monocytes, which require Nr4a1, Bcl6, Irf2, and Cebpb. By comparison, less is known about transcriptional requirements for Ly6Chi monocytes. We find transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα) is highly expressed in Ly6Chi monocytes, but down-regulated in Ly6Clo monocytes. A few previous studies described the requirement of C/EBPα in the development of neutrophils and eosinophils. However, the role of C/EBPα for in vivo monocyte development has not been understood. We deleted the Cebpa +37 kb enhancer in mice, eliminating hematopoietic expression of C/EBPα, reproducing the expected neutrophil defect. Surprisingly, we also found a severe and selective loss of Ly6Chi monocytes, while preserving Ly6Clo monocytes. We find that BM progenitors from Cebpa +37-/- mice rapidly progress through the monocyte progenitor stage to develop directly into Ly6Clo monocytes even in the absence of Notch2 signaling. These results identify a previously unrecognized role for C/EBPα in maintaining Ly6Chi monocyte identity.
논문정보
- Research article
- 2024년 04월 (BRIC 등록일 2024-04-04)
- 국외 연구진
- 생명과학 > 면역학
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