We as a collective human race are discovering so many new and amazing things every single day that it’s easy to believe we can solve every problem.

One of those unsolved mysteries has been how to cure lupus, an autoimmune disease that affects millions of people all over the world.

Now, the discovery of a new immune pathway could mean we’re closer than ever to that being a reality.

Lupus is an autoimmune condition that presents with a range of symptoms like joint and muscle pain, fatigue, rash, headaches, etc.

The variety of symptoms and lack of definitive testing can make a diagnosis hard, but if it’s caught early, treatments work fairly well.

Untreated, or in its most severe forms, it can lead to an early death due to the inflammation of certain organs.

It’s exact cause is up for debate, but we do know that it’s down to problematic interactions between T and B cells, which are part of the immune system.

Patients have high levels of T follicular helper and T peripheral helper cells, which produce a pro-inflammatory molecule called CXCL13.

This attracts B cells, though no one is entirely sure why.

A current course of treatment includes suppressing the immune system so the body stops attacking itself, but as Dr. Jaehyuk Choi explains, it’s not always super effective.

“Up until this point, all therapy for lupus is a blunt instrument. It’s broad immunosuppression.”

But now Choi and his colleagues have identified a pathway in the immune system that appears to drive this process – and not only that, but a way to fix it.

“We’ve identified a fundamental imbalance in the immune responses that patients with lupus make, and we’ve defined specific mediators that can correct this imbalance to dampen the pathologic autoimmune response.”

The pathway is controlled by the aryl hydrocarbon receptor (AHR), which typically functions to help cells respond to environmental stresses like bacteria or pollutants.

When it’s not activated properly, T peripheral helper cells overproduce, which causes an increase in autoantibodies. These are what causes so much trouble lupus patients.

The team tested their hypothesis by taking blood samples from patients with lupus, then added AHR activators into the mix. They saw the T cells reprogram themselves to the Th22 subtype instead of causing inflammation and disease.

This could actually promote healing.

“We found that it we either activate the AHR pathway with small molecule activators or limit the pathologically excessive interferon in the blood, we can reduce the number of the disease-causing cells. If these effects are durable, this may be a potential cure.”

The authors are already working to move on to research that could turn into clinical therapies for real patients.

Music to the ears of millions of people.

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