Re-inventing the wheel with different expensive spokes


Technology is a wonderful thing and allows us to go new places and to go old places to ask the same question with a different tool.

Thirty years ago I collected a number of different anti-macrophage antibodies and did some staining of some EAE tissue and came to the conclusion that there were loads of different subtypes of macrophage or different activation, functional status and things like CD11c, which the immunologists swear is only on dendritic cells where on macrophages and some of the dendritic cell markers were on blood vessels. What could you do with the information, say the immunologists were wrong…yep so not worth the effort so the anwer what do you do and the answer is not a lot.

It was more effort to try and write-up the report. So fast forward thrity years and you have single cell omics and computers and you can get every gene in the genome and you can number crunch and then you get a heatmap and you can say there are different types of macrophages in the brain and if you can throw enough money at the problem hey Voila…Nature paper. Loads of lovely science.

Giladi, A., Wagner, L.K., Li, H. et al. Cxcl10+ monocytes define a pathogenic subset in the central nervous system during autoimmune neuroinflammation. Nat Immunol (2020).

This study sequences monocytes entering the brain of mice and the conlusion is there are many different types and some do damage

A similar approach was done be another group did something similar and said there were different types of microglia.

Mendiola, A.S., Ryu, J.K., Bardehle, S. et al. Transcriptional profiling and therapeutic targeting of oxidative stress in neuroinflammation. Nat Immunol (2020).

They find lots of different monocyte types. They should tie, up Maybe someone can analyse this. Now the question is what does this stuff mean?

Obviously it is all ace. But we have been told from other work that a monocyte/macrophage can change what it secretes as it comes into the CNS so these subtypes are probably stages in development . What does it mean for treatment of MS. Now I shut up, as the effects of modification are hard to work out. My cynical head says I have seen a lot better.

A lot of nice work that would take too long to explain. If the authors follow their altmetric to reach this site, you can write something in plain English for the General public and send to with a picture Bio of yourself and disclaimers. However, they are cherry picking results. In one of the studies they plum for the chronic model of EA, which we have discussed is probably just an asynchronous relapsing model and then they show a treatment effect.

It stops demyelination, however can you smell a fish with what the pictures show, there is no demyelination in the treated group and the lateral columns are shot in the control. But they have had 80 days of damage before treatment starts , so where is it? Sure these are a snap-shot but if they do not reflect the data they represent, whats does it mean?

The stuff I did those many years ago, including the disease inhibition with anti-macrophage agents is destined for the dust bin…Snooze and you loose.

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