‘Bar-coding’ cells reveal new blood origins

Boston – A new way to track cells has revealed some surprising details about the origins of blood. Using a process called cellular “barcode” on mice, researchers from Boston Children’s Hospital found that blood cells don’t come from one type of parent cell – they arise from two types!

They added that their findings could help scientists deal with blood cancers, bone marrow transplants, and also lead to new ways to improve the human immune system.

Principal investigator Fernando Camargo, Ph.D., and a member of the Harvard Stem Cell Institute, says in Media release. “We were surprised to find another group of progenitor cells that don’t come from stem cells. They make most of the blood in a fetus’s life until adulthood, and then they start decreasing gradually.”

The study authors are now working to see if this also applies to human blood cells like that. The new cells, called embryonic pluripotent progenitor cells (eMPPs), could help scientists develop new treatments for elderly adults.

Follow the barcode

The team has been developing this barcode technology for years. Using gene-editing CRISPR or an enzyme known as transposase, the researchers implanted a unique genetic code into the cells of embryonic mice. By doing this, all cells that descend from a cell with a barcode will carry the same genetic sequence – making it easier for scientists to detect them.

Using a cellular barcode allowed the team to monitor all of the different types of blood cells seen in mice, from infancy to adulthood.

“Before, people didn’t have these tools,” Camargo explains. “Also, the idea that Stem Cells It leads to the emergence of all the blood cells implanted in this area so that no one tried to question them. By tracking what happened in mice over time, we were able to see new biology.”

Thanks to this process, the team discovered that eMPPs are actually a more abundant source of lymphocytes than normal blood stem cells. Lymphocytes play a major role in immune responses, including the activity of B cells and T cells. Camargo believes the decrease in eMPPs as a person ages explains why the immune system is there, too It weakens as people age.

“We are now trying to understand why these cells fade away in middle age, which may allow us to manipulate them with a goal immune system regenerationsays the study author.

Scientists think they can achieve this in one of two ways. They can extend the life of eMPP cells using growth factors or immune signaling molecules, or treat blood stem cells with gene therapy — to make them work like eMPPs.

Could this lead to a cure for leukemia?

The study authors add that their breakthrough may lead to a new understanding of how leukemias attack the human body. Specifically, Camargo suspects that myeloid leukemia, which generally affects older patients, may arise from blood stem cells. Meanwhile, lymphocytic leukemia, which develops mainly in children, may arise from eMPPs.

We are following up to try to understand the consequences Mutations that lead to leukemia By looking at their effects in both blood stem cells and eMPPs in mice, he says. “We want to see if the leukemias that arise from these different progenitor cells are different — similar to lymphoid or myeloid.”

Findings related to maternal blood cells may also lead to improvements in bone marrow transplant It is an important procedure in the treatment of leukemia.

“When we tried bone marrow transplants in mice, we found that the eMPPs did not work well; they only lasted a few weeks,” concludes Camargo. If we can add a few more genes to make eMPPs work in the long term, they could potentially be a better source for bone marrow transplantation. They are more common in younger marrow donors than in blood stem cells, and are predisposed to produce lymphocytes, which can lead to better immune reconstitution and reduced post-graft infection complications.”

The results appear in the journal temper nature.