“Inverse Vaccine” Could Treat Multiple Sclerosis and Range of Other Autoimmune Diseases

Mij

Mij

Senior Member (Voting Rights)
Traditional vaccines work by teaching the immune system to recognize a virus or bacteria that needs to be attacked. Now, researchers at the University of Chicago’s Pritzker School of Molecular Engineering (PME) say they have developed a new vaccine that does just the opposite by removing the immune system’s memory of one molecule, an “inverse vaccine” that could be developed to treat multiple sclerosis(MS) and a range of other autoimmune diseases.

https://www.insideprecisionmedicine...erosis-and-range-of-other-autoimmune-diseases
 
Mij said:
Traditional vaccines work by teaching the immune system to recognize a virus or bacteria that needs to be attacked. Now, researchers at the University of Chicago’s Pritzker School of Molecular Engineering (PME) say they have developed a new vaccine that does just the opposite by removing the immune system’s memory of one molecule, an “inverse vaccine” that could be developed to treat multiple sclerosis(MS) and a range of other autoimmune diseases.

https://www.insideprecisionmedicine...erosis-and-range-of-other-autoimmune-diseases
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OMG, bring it on!
 
Wow, this would be incredible if it works. "All" it would take is to identify which antigens are being marked for attack and simply deactivate. Still leaves a lot of work but this could be revolutionary, make autoimmune diseases treatable, even curable.
Achieving that effect for autoimmune diseases, where the immune system attacks a person’s health cells, could halt autoimmune reactions to treat not only MS, but potentially type 1 diabetes, rheumatoid arthritis, Crohn’s disease, and others.
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The new inverse vaccine uses the liver’s method for naturally marking molecules from broken down cells with markers that prevent autoimmune reactions to cells that die via natural processes. To create the vaccine, the PME team assembled an antigen (a molecule being attacked by the immune system), with a molecule that resembles a fragment of an aging cell that the liver would recognize as innocuous. Taking this approach they were able to demonstrate how the vaccine could successfully stop the autoimmune reaction associated with a MS-like disease.
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While the job of the immune system’s T cells is to recognize cells that are foreign to the body and eliminate them, sometimes these cells make mistakes and intend attack normal tissue in the human body. In the case of MS, T cells treat myelin—the protective covering around nerves—as foreign and attacks then; in Crohn’s disease the T cells attack cells in the small intestine.
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The paper.

Synthetically glycosylated antigens for the antigen-specific suppression of established immune responses
https://www.nature.com/articles/s41551-023-01086-2

Inducing antigen-specific tolerance during an established immune response typically requires non-specific immunosuppressive signalling molecules. Hence, standard treatments for autoimmunity trigger global immunosuppression. Here we show that established antigen-specific responses in effector T cells and memory T cells can be suppressed by a polymer glycosylated with N-acetylgalactosamine (pGal) and conjugated to the antigen via a self-immolative linker that allows for the dissociation of the antigen on endocytosis and its presentation in the immunoregulatory environment. We show that pGal–antigen therapy induces antigen-specific tolerance in a mouse model of experimental autoimmune encephalomyelitis (with programmed cell-death-1 and the co-inhibitory ligand CD276 driving the tolerogenic responses), as well as the suppression of antigen-specific responses to vaccination against a DNA-based simian immunodeficiency virus in non-human primates. Our findings show that pGal–antigen therapy invokes mechanisms of immune tolerance to resolve antigen-specific inflammatory T-cell responses and suggest that the therapy may be applicable across autoimmune diseases.​
 
The idea goes back to the 1990s when Herman Waldman tried to tolerate T cells in autoimmunity. But by the end of the 90s we knew that removing T cells completely made no obvious difference. So this looks like a pretty lame duck to me.

And ME looks like it isn't autoimmune so far.

That might be because it actually is a T cell disease but if so almost certainly not autoimmune - so this approach wouldn't work there either.
 
What would a T cell disease look like i.e. in a GWAS [DecodeME]? Any good examples of T cell diseases and have there been GWAS on any of those diseases?
 
psoriasis is a T cell disease, as is ankylosing spondylitis. They show up with linkages to MHC Class I, which is involved in T cell but not B cell recognition interactions. ME does not show Class I linkage but there are lots of other possible candidates.
 
Thank you very much Jonathan (as per all of your contributions).

Possibly psoriasis, & ankylosing spondylitis, have good diagnostic markers/clinical features - so the groups in these GWAS were relatively homogeneous. Possibly/probably ME/CFS is less homogeneous - so more difficult to identify relevant genes & larger [GWAS] studies required - as has been the case in dementia.

EDIT - also, genes well above baseline, but not reaching significance, could still be useful?
 
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Jonathan Edwards said:
psoriasis is a T cell disease, as is ankylosing spondylitis. They show up with linkages to MHC Class I, which is involved in T cell but not B cell recognition interactions. ME does not show Class I linkage but there are lots of other possible candidates.
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That's very interesting. Thinking about the possible hereditary implications found in ME: my father had ankylosing spondylitis, and I've had psoriasis for the last 50 years, 32 years before developing ME. Whereas my mother didn't develop psoriasis until she was 55, shortly before her death.
 
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