Hematopoietic scheme models – why do we need that many?

by Alexey Bersenev on March 1, 2009 · 3 comments

in under discussion

 
Blogging on Peer-Reviewed ResearchA couple of weeks ago we had a journal club about some contradictions in hematopoietic hierarchy models, based on 2 papers –The earliest thymic progenitors for T cells possess myeloid lineage potential from Bhandoola lab and recently published Reductive isolation from bone marrow and blood implicates common lymphoid progenitors as the major source of thymopoiesis from Weissman group.

I would like to remind you that I interviewed Jerimiah Bell – the first author of the paper from Bhandoola lab – how it is going to impact the field. One of the most important conclusions, arising actually from another paper (Wada’s group), published in the same issue of Nature was that their findings:

…argue against the classic model of haematopoiesis in which the common lymphoid progenitors (CLP) is located at the branch point towards T and B-cell lineages, and strongly suggest that the myeloid-based model is applicable to both fetal and adult haematopoiesis.

Well, my opinion is that we should be careful to claim revision of the classical model, because both studies were done in the thymus and we don’t know whether the revision will apply to bone marrow cells. Jerimiah Bell also agreed.

Weissman’s recent paper argues for the myeloid-based model and defends their previously described classic model of hematopoiesis hierarchy. They showed step-by-step that CLPs are the major source of thymocyte progenitors within the BM, which strictly possess lymphoid potential.

Well, Weissman is not giving up! But if you read carefully, you will realize that the work from each lab was done in different cell populations with different methods and techniques. If so how can they contradict with each other? Different cells + different techniques = different results! So there is no contradiction, IMHO.



Moreover, if you look at controversies around models of hematopoiesis hierarchy deeply, you will realize that there are actually more than 2! Yes we have a number of scientific groups and a few models of hematopoiesis in mice. Adding these stories will lead to more controversies. For example – Jacobsen’s model of megakaryocyte-myelopoiesis back in 2005:

legend is available here

So why do we need so many? Why are there differences between the labs? Well the first answer is that no prominent scientist in the field will want to give up but protect their own intellectual property. Secondly, there are so many markers and antibodies for hematopoietic cell detection and so many different techniques to test it – hence, it’s easy to get lost. The same problems exist with markers of hematopoietic cells in human top hierarchy.

Another possible explanation could be that different data from studying the same object is a usual scientific occurence, all within the flow of progress. Or it’s a question of reproducibility – one lab was not able to reproduce results of other (for example why don’t many labs want to use Weissman’s famous Thy1 marker for HSC?) and create their own scheme. But why is it going for a long time? Where is the consensus? Why can’t scientists get together and decide to use the common test systems to finalize the scheme? Well, I don’t think they actually want it. They need to produce papers and multiply young scientists and keep running their own “hematopoietic school”. Will our society benefit from it? I don’t think so. I’m just wondering if someone else feels the same way?

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{ 3 comments… read them below or add one }

Joanna March 1, 2009 at 4:53 am

I think the central problem is that no one has yet shown unequivocal data that 1)explains everything else and 2)is absolutely reliable. Sorting stem cells based on surface markers may not be an absolute test of identity. As long as there is no definitive way to sort cells, there will be quarelling. If all the most prominent scientists in the field met to decide on the best scheme…I think they would not be able to even narrow down the choices at all. :/ Be the one to solve the argument once and for all; find a way around having to know the exact identity of the cell.

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JWS March 1, 2009 at 5:02 am

Unifying these schemes will become important when there is a need for isolating a specific cell population for a therapeutic purpose and if the population isolated by a particular surface phenotype is actually sufficient to generate a desired effect (e.g. which of the MkEP scheme is most effective to generate a large quantity of megakaryocytes for patients with thrombocytopenia, for example?)…

Other than that, it is just about expanding knowledge and it seems that people are not really interested in ‘reconciling’ them, since there is really no need for trying to offend each other by doing so. People have their own criteria and do whatever they can to claim that they are right – there is no value in stirring controversy unless necessary.

In terms of an overall benefit to the society, while integrating different criteria is one way, addressing complexity is another – in the case of complexity like hematopoiesis schemes, the key is how people are going to represent this complexity.

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Alex March 2, 2009 at 5:02 pm

to Joanna –
yes finding exact cell identity is tough, but I think flow cytometry the best way to sort them out so far. If you know better, please share.

to JWS –
yes, I’d agree that unifying schemes will be very important for clinical applications. This is exactly my point. Basic science is interesting too, but not too much. Making a bubble for no reason is not good.

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