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Image by Andre E.X. Brown
Preclinical research appears to explain how the body can quickly replenish platelets that are lost during infection.
Investigators discovered an “emergency backup system” in mice that bypasses the known pathway of hematopoietic stem cell (HSC) differentiation so that platelet numbers can be restored rapidly.
Marieke Essers, PhD, of The German Cancer Research Center (Deutsches Krebsforschungszentrum) in Heidelberg, Germany, and her colleagues described this phenomenon in Cell Stem Cell.
The team discovered a small cell population within the HSC compartment that induces differentiation in megakaryocytes.
These quiescent stem cells—dubbed stem-like megakaryocyte-committed progenitors (SL-MkPs)—do not provide the normal supply of platelets but serve as a backup in case of emergency.
When quiescent, SL-MkPs express few proteins. In the event of an acute infection, SL-MkPs are aroused from their quiescent state by interferon α, express the typical megakaryocyte proteins, and are rapidly differentiated into advanced precursor cells.
This quickly replaces the platelets that were lost as a result of the infection.
This emergency backup system bypasses the lengthy process of normal HSC differentiation, thereby ensuring that any life-threatening loss of platelets is compensated for quickly.
However, the investigators found that repeat infections can result in the reservoir of SL-MkPs being depleted. 
Image by Andre E.X. Brown
Preclinical research appears to explain how the body can quickly replenish platelets that are lost during infection.
Investigators discovered an “emergency backup system” in mice that bypasses the known pathway of hematopoietic stem cell (HSC) differentiation so that platelet numbers can be restored rapidly.
Marieke Essers, PhD, of The German Cancer Research Center (Deutsches Krebsforschungszentrum) in Heidelberg, Germany, and her colleagues described this phenomenon in Cell Stem Cell.
The team discovered a small cell population within the HSC compartment that induces differentiation in megakaryocytes.
These quiescent stem cells—dubbed stem-like megakaryocyte-committed progenitors (SL-MkPs)—do not provide the normal supply of platelets but serve as a backup in case of emergency.
When quiescent, SL-MkPs express few proteins. In the event of an acute infection, SL-MkPs are aroused from their quiescent state by interferon α, express the typical megakaryocyte proteins, and are rapidly differentiated into advanced precursor cells.
This quickly replaces the platelets that were lost as a result of the infection.
This emergency backup system bypasses the lengthy process of normal HSC differentiation, thereby ensuring that any life-threatening loss of platelets is compensated for quickly.
However, the investigators found that repeat infections can result in the reservoir of SL-MkPs being depleted.
Image by Andre E.X. Brown
Preclinical research appears to explain how the body can quickly replenish platelets that are lost during infection.
Investigators discovered an “emergency backup system” in mice that bypasses the known pathway of hematopoietic stem cell (HSC) differentiation so that platelet numbers can be restored rapidly.
Marieke Essers, PhD, of The German Cancer Research Center (Deutsches Krebsforschungszentrum) in Heidelberg, Germany, and her colleagues described this phenomenon in Cell Stem Cell.
The team discovered a small cell population within the HSC compartment that induces differentiation in megakaryocytes.
These quiescent stem cells—dubbed stem-like megakaryocyte-committed progenitors (SL-MkPs)—do not provide the normal supply of platelets but serve as a backup in case of emergency.
When quiescent, SL-MkPs express few proteins. In the event of an acute infection, SL-MkPs are aroused from their quiescent state by interferon α, express the typical megakaryocyte proteins, and are rapidly differentiated into advanced precursor cells.
This quickly replaces the platelets that were lost as a result of the infection.
This emergency backup system bypasses the lengthy process of normal HSC differentiation, thereby ensuring that any life-threatening loss of platelets is compensated for quickly.
However, the investigators found that repeat infections can result in the reservoir of SL-MkPs being depleted.