New Research that re-educates the immune system

Arthuritis

Also…

Professor Ranjeny Thomas 

Arthritis Qld Chair of Rheumatology

Frazer Institute

Faculty of Medicine

Professor Thomas’ research is focused on the study of the biology and clinical use of human dendritic cells in autoimmune disease. It has explored basic mechanisms of immunity and dendritic cell function in autoimmune disease.

Her research is focussed on the study of autoimmune disease and restoration of tolerance. Through this work, she developed and tested the first rheumatoid arthritis vaccine. She has also contributed major insights into the pathogenesis of spondyloarthropathy and autoimmune diabetes, leading to the development of disease biomarkers and innovative immunotherapies.

Research Impacts

1. Antigen-specific immunotherapy. My team and I developed and have a granted patent for a liposome immunotherapy strategy to induce antigen-specific tolerance in rheumatoid arthritis (RA). It is the first to specifically target ACPA autoantibody-positive patients carrying RA-susceptibility gene variants, each identifiable with existing tests. The product, DEN181 was developed by Dendright, the Uniquest spin-off company founded to commercialize the liposome technology, in partnership and option to licence with Janssen-Biotech, the US pharmaceutical subsidiary of Johnson and Johnson, for the indication of RA. DEN-181 completed a single-dose ascending phase 1 clinical trial in RA at PA Hospital in 2019 (PI – Phillip Vecchio). Mechanistic pre-clinical studies were published in Galea et al, JCI Insight 2019.

2. To translate antigen-specific immunotherapy to children with type 1 diabetes, we carried out pre-clinical studies with Emma Hamilton-Williams and Mark Harris. I am PI on a grant to this team from JDRF and the US Leona M. and Harry B. Helmsley Charitable Trust for a clinical trial of liposomes encapsulating NF-kB inhibitor and diabetes-specific peptide in patients with T1D. We are currently undertaking pre-clinical development. Mechanistic pre-clinical studies were published in Bergot et al, J Immunol 2020.

Louisa77

Thanks for sharing - do take a look at the research we are funding

https://www.versusarthritis.org/news/?CategoryId=53260

Arthuritis

@Louisa77 Thanks I did take a look, but there is no VA research I could find on:

1. Reactive arthritis masquerading as Rheumatoid. It has the same serology, but unlike Rheumatoid, if the trigger antigen is removed, the symptoms go away. The trigger is often gut disease related or a drug. GI consultants often see this with IBD, where if the suppression is excessive it leads to overgrowth of gut bacteria that trigger flares. GI consultants treat this with antibiotics. Gingivitis (dental), Lyme disease & some STDs also have the same RA symptoms and serology. I did see a little bit of sponsorship of the Kennedy institute’s research where Prof Venables wrote an article in the BMJ about gum disease leading to RA as the bacteria can trigger an RA flare. Not much discussion here about possible causes as a differential diagnosis. It is just assumed to be rheumatoid. However if the cause is bacterial suppression just perpetuates the disease or makes it worse. Which leads to the question; how many patients might there be assumed to have rheumatoid, when there might be an underlying infection causing this?
2. Additionally there is no research mentioned along the lines of Nobel prize winner Dr Barry Marshall, who rocked the boat of conventional wisdom that incurable chronic painful gastric ulcers are caused by lifestyle choices, the “stressed businessman’s disease”. Today it is accepted that the cause is a bacterium, but when Marshall first raised it he was ostracised by pharma and the med community who relied on the steady income from the profitable sales of expensive PPIs & Antacids. Medical Research is a science that requires challenge, not a religion.

A senior rheumatologist at a major London hospital told me that there isn’t any funding for a cure because there is no incentive for the pharmas to fund that, which is a huge shame. While the majority of rheumatoid arthritis sufferers will have genuine autoimmune disease, I am certain there are a good number who have reactive arthritis with a treatable trigger.

I hope someday funding for curative research will not unexpectedly dry up the moment their research becomes prominent or close to a repeat of Dr Marshall’s findings.