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Updated: Nov 24, 2025

Phenotypic Analysis and Isolation of Murine Hematopoietic Stem Cells and Lineage-committed Progenitors
Published on: July 8, 2012
CD11c regulates hematopoietic stem and progenitor cells under stress
Lifei Hou1,2,3, Richard A Voit4,5, Vijay G Sankaran4,5
1Cardiac Anesthesia Division, Department of Anesthesiology, Critical Care and Pain Medicine, Boston Children's Hospital, Boston, MA.
CD11c, a beta-2 integrin, is expressed on hematopoietic stem and progenitor cells (HSPCs). Its deficiency causes HSPC loss during stress, revealing a distinct role beyond its dendritic cell marker function.
Area of Science:
- Immunology
- Hematology
- Cell Biology
Background:
- Beta-2 integrins (CD11a-d) are key leukocyte adhesion molecules.
- Research has primarily focused on CD11a and CD11b, with CD11c's function less characterized.
- CD11c is known as a dendritic cell marker but its role in other cell types is limited.
Purpose of the Study:
- To investigate the expression and function of CD11c in hematopoietic stem and progenitor cells (HSPCs).
- To determine the role of CD11c in HSPC regulation, particularly under stress conditions.
- To elucidate the impact of CD11c deficiency on HSPC survival and expansion.
Main Methods:
- Analysis of CD11c expression on hematopoietic stem and progenitor cells (HSPCs).
- Phenotypic characterization of HSPCs in CD11c knockout mice under normal conditions.
- Assessment of HSPC numbers and apoptosis in CD11c deficient mice during sepsis and bone marrow transplantation models.
Main Results:
- CD11c is expressed on short-term HSPCs and multipotent progenitor cells.
- CD11c deficiency did not impact HSPC numbers in healthy mice.
- CD11c deficiency led to increased apoptosis and significant loss of HSPCs in sepsis and bone marrow transplantation models.
Conclusions:
- CD11c plays a distinct role in regulating HSPC expansion under stress, unlike other beta-2 integrins.
- CD11c is expressed on HSPCs and functions as a critical regulator of their survival during stress.
- CD11c deficiency results in HSPC loss through apoptosis in conditions like sepsis and bone marrow transplantation.
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