Scientists have found a way to block the inflammation caused by rheumatoid arthritis

(ORDO NEWS) — A team of researchers in the United States has discovered a new mechanism in which a key protein causes inflammatory damage associated with rheumatoid arthritis.

It is expected that this fundamental discovery will direct research into entirely new ways to treat an autoimmune disease that affects millions of people.

One of the most important discoveries in the field of rheumatoid arthritis over the past few decades has been the discovery of an immune cytokine called tumor necrosis factor-alpha (TNF-alpha), which plays a critical role in joint tissue inflammation.

Since this discovery, the development of TNF inhibitor monoclonal antibodies has offered rheumatoid arthritis patients an entirely new type of drug to treat their condition.

But as senior author of the new study, Salah-Uddin Ahmed, explained, TNF inhibitors are not effective in all patients. And even then, they are not ideal long-acting drugs because of the many side effects.

“Tumor necrosis factor-alpha or TNF-alpha for short is one of the main inflammatory proteins that causes rheumatoid arthritis, and many of the treatments currently available are targeting it,” Ahmed said.

“However, over time, patients may develop resistance to these drugs, meaning they no longer have an effect on the body.

That’s why we were looking for previously unknown drug targets in TNF-alpha signaling, which are basically proteins that the factor interacts with.”

The new laboratory study focused on a type of human cell called synovial fibroblasts. These are the cells that line the joints, and in cases of rheumatoid arthritis, inflammation of the synovial fibroblasts is triggered by TNF-alpha.

Experimental results

In the search for a protein that plays a role in joint inflammation, the researchers focused on a molecule called sulfatase-2. Previous cancer research has shown that sulfatase-2 plays a role in tumor growth and is known to be involved in immune cell signaling processes.

Thus, the researchers hypothesized that sulfatase-2 may play a role in how TNF-alpha causes inflammation.

To test this, the team removed a protein from synovial fibroblasts and then observed what happened when the cells were stimulated with TNF-alpha. Interestingly, as a result, experiments have shown a significant reduction in inflammatory responses in cells.

It is important to note that this research is still at a very early stage. These results have so far only been established in cellular models and further animal studies will be required to test these mechanisms before any kind of human treatment can be considered.

Nevertheless, this is an extremely promising fundamental discovery. In addition, there is other work aimed at blocking sulfatase-2 to treat cancer.

In fact, the sulfatase-2 inhibitor is already in Phase 2 human clinical trials as a treatment for severe brain cancers, so if this mechanism is further confirmed in rheumatoid arthritis, it may be possible that trials will begin at an accelerated pace – and after them in pharmacies will also have affordable drugs.


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