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in the bone marrow
By assigning a “barcode” to hematopoietic stem cells (HSCs), researchers have found they can monitor the cells and study changes that occur over
time.
In tracking the barcoded HSCs, the team discovered why B-1a cells develop primarily during fetal and neonatal life, while adult bone marrow HSCs preferentially give rise to B-2 cells.
Joan Yuan, PhD, of Lund University in Sweden, and her colleagues described this discovery in Immunity.
“By assigning a barcode to the stem cells, we were able to track their performance over long periods of time and see which cells in the blood and the immune system they can induce,” Dr Yuan explained.
“Without the barcode, we only see a bunch of red and white blood cells, without knowing how they are related. This allows us to track which stem cell has given rise to which subsidiary cells and thereby distinguish the ‘family tree’ in the blood.”
In this way, the researchers found that B-1a cells and B-2 cells have a shared precursor in the fetal liver. And definitive fetal liver HSCs gave rise to both B-1a and B-2 cells. However, over time, the HSCs were not able to maintain B-1a output.
“The same stem cells exist within adults [and fetuses], but they have lost their ability to regenerate the entire immune system [in adulthood],” said study author Trine Kristiansen, a doctoral student at Lund University.
“By adding a protein normally only found in the stem cells of a fetus, we were able to reconstruct [the HSCs’] capacity to produce white blood cells.”
The researchers restored the HSC’s ability to produce B-1a cells by inducing expression of the RNA binding protein LIN28B, which regulates fetal hematopoiesis.
The team said these results suggest the decline in regenerative potential is a reversible state for HSCs. The researchers believe this finding could have implications for the treatment of blood disorders and particularly for HSC transplant.
“In this treatment, the patient’s blood system is replaced with that of an adult donor, which could mean losing the B cells that are only produced in fetuses,” Kristiansen said.
Without these cells, a person is at risk of developing immune system disorders that can lead to severe infections and autoimmune diseases.
“Every day, millions of blood cells die, and they can emit DNA and other debris that cause inflammation if not taken care of by the white blood cells,” said study author Elin Jaensson Gyllenbäck, PhD, of Lund University.
“The discovery is a step towards understanding which processes create a proper immune system for those who suffer from blood diseases.” 
in the bone marrow
By assigning a “barcode” to hematopoietic stem cells (HSCs), researchers have found they can monitor the cells and study changes that occur over
time.
In tracking the barcoded HSCs, the team discovered why B-1a cells develop primarily during fetal and neonatal life, while adult bone marrow HSCs preferentially give rise to B-2 cells.
Joan Yuan, PhD, of Lund University in Sweden, and her colleagues described this discovery in Immunity.
“By assigning a barcode to the stem cells, we were able to track their performance over long periods of time and see which cells in the blood and the immune system they can induce,” Dr Yuan explained.
“Without the barcode, we only see a bunch of red and white blood cells, without knowing how they are related. This allows us to track which stem cell has given rise to which subsidiary cells and thereby distinguish the ‘family tree’ in the blood.”
In this way, the researchers found that B-1a cells and B-2 cells have a shared precursor in the fetal liver. And definitive fetal liver HSCs gave rise to both B-1a and B-2 cells. However, over time, the HSCs were not able to maintain B-1a output.
“The same stem cells exist within adults [and fetuses], but they have lost their ability to regenerate the entire immune system [in adulthood],” said study author Trine Kristiansen, a doctoral student at Lund University.
“By adding a protein normally only found in the stem cells of a fetus, we were able to reconstruct [the HSCs’] capacity to produce white blood cells.”
The researchers restored the HSC’s ability to produce B-1a cells by inducing expression of the RNA binding protein LIN28B, which regulates fetal hematopoiesis.
The team said these results suggest the decline in regenerative potential is a reversible state for HSCs. The researchers believe this finding could have implications for the treatment of blood disorders and particularly for HSC transplant.
“In this treatment, the patient’s blood system is replaced with that of an adult donor, which could mean losing the B cells that are only produced in fetuses,” Kristiansen said.
Without these cells, a person is at risk of developing immune system disorders that can lead to severe infections and autoimmune diseases.
“Every day, millions of blood cells die, and they can emit DNA and other debris that cause inflammation if not taken care of by the white blood cells,” said study author Elin Jaensson Gyllenbäck, PhD, of Lund University.
“The discovery is a step towards understanding which processes create a proper immune system for those who suffer from blood diseases.”
in the bone marrow
By assigning a “barcode” to hematopoietic stem cells (HSCs), researchers have found they can monitor the cells and study changes that occur over
time.
In tracking the barcoded HSCs, the team discovered why B-1a cells develop primarily during fetal and neonatal life, while adult bone marrow HSCs preferentially give rise to B-2 cells.
Joan Yuan, PhD, of Lund University in Sweden, and her colleagues described this discovery in Immunity.
“By assigning a barcode to the stem cells, we were able to track their performance over long periods of time and see which cells in the blood and the immune system they can induce,” Dr Yuan explained.
“Without the barcode, we only see a bunch of red and white blood cells, without knowing how they are related. This allows us to track which stem cell has given rise to which subsidiary cells and thereby distinguish the ‘family tree’ in the blood.”
In this way, the researchers found that B-1a cells and B-2 cells have a shared precursor in the fetal liver. And definitive fetal liver HSCs gave rise to both B-1a and B-2 cells. However, over time, the HSCs were not able to maintain B-1a output.
“The same stem cells exist within adults [and fetuses], but they have lost their ability to regenerate the entire immune system [in adulthood],” said study author Trine Kristiansen, a doctoral student at Lund University.
“By adding a protein normally only found in the stem cells of a fetus, we were able to reconstruct [the HSCs’] capacity to produce white blood cells.”
The researchers restored the HSC’s ability to produce B-1a cells by inducing expression of the RNA binding protein LIN28B, which regulates fetal hematopoiesis.
The team said these results suggest the decline in regenerative potential is a reversible state for HSCs. The researchers believe this finding could have implications for the treatment of blood disorders and particularly for HSC transplant.
“In this treatment, the patient’s blood system is replaced with that of an adult donor, which could mean losing the B cells that are only produced in fetuses,” Kristiansen said.
Without these cells, a person is at risk of developing immune system disorders that can lead to severe infections and autoimmune diseases.
“Every day, millions of blood cells die, and they can emit DNA and other debris that cause inflammation if not taken care of by the white blood cells,” said study author Elin Jaensson Gyllenbäck, PhD, of Lund University.
“The discovery is a step towards understanding which processes create a proper immune system for those who suffer from blood diseases.”