Cutting-Edge RA Research: What’s Hot & What It Means for You

RA Research

When you read about hot research discoveries about rheumatoid arthritis in the news, you may think…what does this mean for me and my disease? Are there groundbreaking new treatments or even a cure for RA on the horizon?

RA research is incredibly exciting and promising right now? Scientific discovery is a pretty slow process. Breakthroughs in laboratories point the way to life-changing therapies down the road, but they often face years of tests and clinical trials. The RA medications that you take to manage your symptoms and control your inflammation are the result of scientific research that took place decades ago. 

Breakthroughs Are a Long Journey

The road to effective therapy for RA and other diseases begins with what’s called basic science research. Before drugs can be developed and manufactured to block the processes of inflammation and joint damage in your body, scientists had to figure out why those processes happen in autoimmune diseases like RA. Once they understood more about how and why RA works, then they developed drugs that targeted the sources of inflammation to prevent joint damage and disease progression. 

Today, even more, exciting studies are building on the discoveries of the past. RA researchers are now able to pinpoint unique cells that play a role in RA inflammation. This information may lead to new, incredibly powerful RA treatments or maybe even a cure for RA. It all starts in the lab with tests on mice.

Unique Immune Cells in RA: Possible Clue to a Cure?

One of the hottest new studies in rheumatoid arthritis was published this summer by researchers at Stanford University School of Medicine in the journal Nature Immunology. They were able to block inflammation and tissue damage caused by RA in mice1. These were no ordinary mice, but animals specially bred and adapted for the study: they had human synovium, or joint lining, grafted onto their little joints, and “humanized” adapted immune systems. 

The researchers were able to identify a faulty mechanism in humans with RA, then shut that mechanism off in the mice to block inflammation and damage. They also found that an experimental drug called A769662, which hasn’t been tested in clinical trials yet, could protect immune cells from RA’s destruction.

What the study found:

The researchers identified an important immune cell in RA called the helper T cell. 

The researchers found that helper T cells in people with RA act differently than they do in people without the disease.

People with RA have low levels of ATP, an energy source for cells. Instead of building more ATP to make up for the shortfall, the immune systems of people with RA feed energy into other types of cells that cause damage in joints. This process is usually regulated by a molecule called AMPK. But in RA, AMPK fails to perform its usual role and helper T cells grow out of control. When everything is working as it should, AMPK molecules bind to the surfaces of lysosomes–very tiny organs that act to clean out the “garbage” in your body’s cells–and activate a process to keep your ATP levels healthy. In people with RA, that’s not happening, they found.

They extracted helper T cells from the blood of people with RA to study how the cells behaved. They discovered that people with RA have the same levels of AMPK in their blood as those without the disease, their AMPK never “switches on” for some reason. They also found that people with RA have helper T cells with very low levels of an enzyme called NMT1, which allows AMPK to do its job in your immune system.

When they injected helper T cells from the blood of people with RA into the mice, the result was bad: inflammation and severe synovium damage. But when they injected the mice with helper T cells modified to have boosted NMT1 levels, the animals had far less inflammation and damage. They also learned that the experimental drug, A769662, could “switch on” AMPK in RA, and hope to begin clinical trials of this treatment soon to learn more about how it works, and if it’s safe to use in humans.

Why Drug Discovery Takes So Long

Why can’t people with RA go ahead and try A769662 (which is so new it doesn’t even have a name) now to see if it will work to reverse their disease? Because it takes many years to put new treatments through the necessary testing and clinical trials to determine that it’s safe and effective for your body. Just because a drug works in mice or even in a lab dish doesn’t mean that it will work in a human. 

What can you do in the meantime?

There’s a lot you can do today to manage your RA disease activity and feel better. Stick to your treatment plan. Stay physically active, don’t smoke, eat a healthy and balanced diet, and follow your Vectra Score to track your RA disease activity over time. Vectra Score is an advanced blood test that measures RA inflammatory disease activity in  a unique way, combining 12 blood biomarkers into one score on a scale of 1-100. If your Vectra Score is low and stays that way, you’re at lower risk for joint damage in the future. 

Talk with your rheumatologist about your Vectra Score and keep track of any changes over months or years. You can get your Vectra Score anytime via your personalized myVectra patient portal online, or on your MyVectra app on your smartphone or tablet. 


  1. Wen Z, Jin K, Shen Y, et al. “N-myristoyltransferase deficiency impairs activation of kinase AMPK and promotes synovial tissue inflammation.” Nat Immunol. 2019 Feb;20:313-325.
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