PD-1: New target molecule to halt aberrant dendritic cells!

[serg1942]

Hi everybody,

A fellow just showed me this study, and I think it is really interesting. They have found a molecule expressed in the dendritic cells, strongly related to their apoptosis. If this molecule works the same way in humans, then a drug to inhibit it could allow us to induce the apoptosis of dendritic cells, hence halting their aberrant behavior recently found in ME/CFS, via the human endoretroviruses. In other words, by inhibiting this molecule, it would be plausible to lower the chronic inflammation, non-specific T cell proliferation, autoimmunity, etc, that could be behind the symptoms of ME/CFS.

I think this kind of drugs, together with monoclonal antibodies that are being already tried in MS (http://forums.phoenixrising.me/index.php?threads/new-drug-for-ms-in-phase-2-possible-new-treatment-for-cfs-gnbac1-against-msrv.29717/) could be the new and most hopeful drugs we may soon have available. (Actually, I do thing the monoclonal antibodies, much more than drugs killing a whole kind of immune cells, are the real "antibiotics" of the future, of course much more specific, efficient and with many less side effects).

http://www.jleukbio.org/content/95/4/621

Best!
Sergio

 

[anciendaze]

Sounds very interesting, but I have to caution that we are talking about rather drastic modifications of immune function. It is quite possible to do harm by unselective treatments. Experience in the treatment of cancer and autoimmune disease indicates you need very specific targeting, usually with multiple markers. It took 20 years to reach this degree of selectivity in treatment of some cancers. Other cancers remain hard to treat, and a friend of mine appears close to dying this weekend because this has not been done for his particular disease.

 

[serg1942]

Of course, that's why I prefer the monoclonal antibodies against 1 specific protein. But, even a drug that induces apoptosis of non specific dendritic cells, could actually stop our symptoms. Kind of what rituximab did, but with the advantage of killing the possible --let's say KDM and Lombardi's work is confirmed-- cells causative of the disease by expressing HERVs proteins. These cells are not working well anyway. Also, we do have other professional antigens presenting cells that could take over this task, at least for part of it. And maybe, by modulating the rate of apoptosis of DCs, we could successfully kill the pathogens activating them.

I see this more specific than killing all your B cells. But yes, of course the main obstacle here as you say is the specificity of the drug.

Best!
Sergio

 

[Valentijn]

@serg1942 - Could you please not color the text of your entire posts? I use a dark theme because I have trouble with the light themes, and colored text tends to look pretty awful

 

[serg1942]

Hi @Valentijn , I am sorry, I didn't know about the dark theme... Sure, no problem!

Sergio