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The way we treat autoimmune diseases is rapidly changing
“One of the most ground-breaking things that has happened,” one researcher says.
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If you get arthritis, lupus or multiple sclerosis (MS), it means that your body is turning its own defences against you. Every time the disease flares up, an army of white blood cells attacks joints, connective tissue or nerve cells.
Steroids and other drugs that reduce inflammation have been an obvious treatment for these types of autoimmune diseases.
But in recent years, research has pointed in a new direction.
The focus has shifted to removing a specific type of white blood cells. They are called B cells.
“One of the most ground-breaking things that has happened”
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“If you look at the synovial fluid of someone with arthritis or the spinal fluid of someone with MS, there are very few B cells. So you might not think it would be that effective to remove them,” says Asbjørn Christophersen.
He is a senior physician at Oslo University Hospital and does research on rheumatic diseases at the University of Oslo.
The role of B cells is actually to alert the body to invaders such as viruses and bacteria and to make antibodies against them.
But in people with autoimmune diseases, these cells also raise an alert to cells in your own body. That makes your immune system perceive parts of your body as dangerous.
Removing the B cells that drive this process has been shown to work against many different autoimmune diseases.
“It is one of the most ground-breaking things that has happened in rheumatology and neurology,” says Andreas Lossius, who does research on a variety of autoimmune diseases at the University of Oslo.
Immunotherapy has become more sophisticated
One example is MS. In this case, these drugs halt the inflammation that results from autoimmune attacks in many MS patients and have improved their prognosis.
This is particularly the case if the diagnosis is made early and treatment starts immediately.
These drugs are antibodies that direct the immune system to bind to the B cells. They are kind of a flag that alerts the body to danger.
These antibodies, both against B cells and other parts of the immune system, are also used to treat arthritis, among other illnesses.
But not only that. In recent years, the drugs that target these cells have become even more sophisticated.
Two different therapies do much of the same thing
One of the treatments is called CAR-T. Thu-Tao and several other lupus patients have become symptom-free (article in Norwegian) after treatment with this immunotherapy.
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A woman with three different autoimmune diseases also almost recovered after receiving the treatment.
This is a treatment that uses living cells. The most common approach uses your own T cells which are harvested from your blood and genetically modified. The T cells then are experts at killing other cells. When they are put back into your body, they have been programmed to attack B cells.
But this is not the only promising new medicine.
A simpler type of immunotherapy, which does much of the same thing in the body, has also emerged as a possible alternative.
These are called bispecific antibodies.
Forced close together
These drugs bind to two different cells at once.
While traditional antibodies depend on a killer cell passing by and discovering that the B cell has been flagged as dangerous, this is not needed for the new medicines, explains Lossius.
Bispecific antibodies actually grab hold of both a B-cell and a T-cell. In this way, they are forced so close together that the B cell is killed.
“So it is a more effective way of killing the B cells than ordinary antibodies,” says Lossius.
These drugs have shown good effects against several types of cancer, including for patients with bone marrow cancer (in Norwegian).
Six patients quickly got much better
And in recent years, studies have emerged which suggest that these medicines can also benefit patients with autoimmune diseases.
In a study published in Nature Medicine in 2024, six patients with arthritis, who did not respond to any other medication, received this kind of immunotherapy.
This was a variant of bispecific antibodies called Bispecific T-cell engager (BiTE).
All the patients rapidly improved after treatment.
But many questions remain before these drugs can be rolled out for a larger number of patients with autoimmune diseases.
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Developed an acute inflammatory condition
There aren’t many studies of these drugs, and all are small. And the medicines are not necessarily harmless.
For example, a study published in Nature Medicine in February 2026 describes five patients with systemic sclerosis and five patients with the muscle disease antisynthetase syndrome.
All were treated with BiTE as a last resort.
But although most of them recovered significantly from the immunotherapy, the majority also experienced unwanted side effects. Several experienced an acute inflammatory condition called a cytokine storm.
A woman with lupus who received treatment with a different type of bispecific antibody also experienced this problem, according to a study from 2024 in The New England Journal of Medicine.
At the same time, the researchers describe the effect as remarkable. The 23-year-old woman became completely symptom-free after the treatment.
Very exciting
So which patients can get BiTE or other types of bispecific antibodies?
Initially, Christophersen says, it will only be appropriate to give these medications when doctors have no other options.
That is, when doctors have tried all other treatments or when the disease worsens very quickly and the patient is at risk of dying.
“It is very exciting that we can now perhaps start to help those patients whose rheumatic condition progresses very rapidly,” Christophersen said.
At Oslo University Hospital, one patient with very serious autoimmune rheumatic disease has recently received BiTE treatment, he said.
The decision to treat was made after careful consideration by the rheumatologists and haematologists at the hospital, and the treatment required permission from the hospital director.
Increased likelihood of more frequent infections
But this involves a great deal of responsibility related to the risk of infection in particular, Christophersen said.
Research shows that patients who receive these medications have a much greater risk of developing infections. That’s not so surprising, given that the medications knock out all B cells.
This means only those B cells cause the immune system to attack itself, but also those that alert the body to dangerous viruses and bacteria.
As a result, each patient must be assessed individually, Christophersen points out.
Uncertain which is best
At the same time, it is also unclear which is the more effective of the two immunotherapies, CAR-T or bispecific antibodies and BiTE.
Lossius is in favour of CAR-T, which with its live cell therapy is now being tested against MS.
A possible advantage is that the CAR-T cells themselves can migrate into the tissues and seek out B cells there, he points out.
But bispecific antibodies have several practical advantages. They do not need to be adapted to each individual patient, do not require special laboratories and can be given as a syringe right away.
Starting with stronger drugs
Regardless, people are thinking differently now about the treatment of autoimmune diseases, the researchers say.
“In neurology, there has probably been a shift in the way we look at these things in the last ten to twenty years. Previously, we were perhaps more cautious about treating patients with very strong medications early on,” says Lossius.
“Now, we start much earlier with medications that have a very good effect, but which can also potentially have side effects,” he said.
The same applies in rheumatology, Christophersen said.
References:
L. Bucci et al.:, Bispecific T cell engager therapy for refractory rheumatoid arthritis. Nature Medicine, April 2024.
C. Düsing et al.: Bispecific T cell engagers for treatment-refractory autoimmune connective tissue diseases. Nature Medicine, February 2026.
T. Alexander et al.: Teclistamab-Induced Remission in Refractory Systemic Lupus Erythematosus. The New England Journal of Medicine, September 2024.
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Translated by Nancy Bazilchuk
Read the Norwegian version of this article at forskning.no
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