Recently I’ve questioned why do we have so many models of hematopoietic hierarchy? It’s getting even more and more complicated over the years. Last week I just came across a fresh review of this topic, prepublished online in Nature Review Immunology – Models of haematopoiesis: seeing the wood for the trees by Rhodri Ceredig, Antonius G. Rolink & Geoffrey Brown. I’d like to share it with you here because I like their model and discussion.
Some of this confusion may be because there is a difference between what occurs in vivo and what HSCs can be ‘persuaded’ to do in vitro. We think that the traditional hierarchical tree may not be the best way to illustrate haematopoiesis. Hence, we explore an alternative view to explain how intermediate progenitors can give rise to certain combinations of cell fates while excluding others.
In the pairwise relationships model there are no assumptions about any underlying strict branching pattern that might seem to dictate a preferred route for HSCs to a particular cell fate. In other words, HSCs can reach a specific cell fate through more than one type of intermediate progenitor.
To me the circle-like model looks reasonable and logical. The authors also provide a good map of transcription factor – regulators of hematopoiesis, which fit very well to their pairwise model. But it seems like mapping of surface markers will be not that easy, likely blurring the picture.
explanation in dendritic lineage example:
…In this regard, subsets of DCs can be derived from cells purified as either CLPs or common myeloid progenitors (CMPs), suggesting that DCs can have both lymphoid and myeloid origins. However, the cell surface phenotypes and transcriptional profiles of DC subsets derived from different progenitors appear to be identical, so it seems that the developmental programme of DCs is independent from that of lymphoid and myeloid cells…
if you would like to read the article, ask me