Category: Research and Discovery

The work was led by scientists at NHS Blood and Transplant in Bristol, including researchers from the International Blood Group Reference Laboratory (IBGRL), together with colleagues at the University of Bristol. Their findings solved a puzzle dating back to 1972 and could help prevent dangerous transfusion reactions in a small number of patients.

Although most people are familiar with the ABO and Rh blood groups, those are only part of a much larger biological system. Red blood cells carry hundreds of different molecules on their surfaces. Many of these molecules act as antigens, markers that the immune system can recognize.

For most transfusions, ABO and Rh compatibility receive the most attention. But in patients with unusual antibodies or rare blood types, matching some of these lesser-known antigens can become crucial.

A Blood Marker Found in More Than 99.9% of People

The AnWj antigen was discovered in 1972, but for decades scientists did not know which gene produced it or which protein carried it on red blood cells.^[1]

More than 99.9% of people are AnWj positive. For the tiny minority who are AnWj negative, however, the distinction can matter enormously.

If an AnWj negative person develops antibodies against AnWj and then receives AnWj positive blood, those antibodies can attack the transfused red blood cells. In some circumstances, that can trigger a potentially serious transfusion reaction.

There are also two very different reasons someone can lack the antigen. In most cases, AnWj expression appears to be suppressed because of an underlying hematological disorder or certain cancers.^[2] Much more rarely, a person is born without the antigen because of an inherited genetic change.

Only a handful of people with this inherited form had ever been identified, making the mystery especially difficult to investigate.

The Genetic Clue Was Hidden in MAL

To find the source, the researchers turned to whole exome sequencing. This technique examines the portions of DNA that contain instructions for making proteins, allowing scientists to search across thousands of genes for unusual variants shared by affected individuals.

The analysis pointed unexpectedly to the MAL gene.

The researchers found that people with the inherited AnWj negative phenotype carried homozygous deletions affecting MAL. Homozygous means that the relevant change was present in both copies of the gene, one inherited from each parent.

The MAL gene produces a small membrane protein called Mal. When the team examined red blood cells, people who were AnWj positive produced the full-length Mal protein on their cells, while it was missing from AnWj negative cells.

Five genetically AnWj negative individuals were included in the investigation, including members of an Arab Israeli family.^[3] The samples also included blood donated in 2015 by the woman who had been the first AnWj negative person identified in the 1970s.

The researchers did not stop at finding a genetic association. They needed to demonstrate that Mal really was responsible for the antigen.

When scientists introduced the normal MAL gene into laboratory cells, the cells became reactive with AnWj antibodies. Introducing the altered form did not produce the same response. Additional experiments showed that Mal was both necessary and sufficient for expression of the AnWj antigen.

MAL Becomes an Official Blood Group System

Those results provided the evidence needed to establish MAL as a distinct blood group system, with AnWj as its defining antigen.

The International Society of Blood Transfusion later formally reported MAL as ISBT 047. MAL was one of four blood group systems ratified during the period covered by the organization’s 2026 terminology report, alongside ER, CD36 and ATP11C.

That designation is more significant than simply adding another name to a list. For something to qualify as a blood group system, researchers must connect an antigen to a defined genetic and molecular basis.

MAL was the 47th officially recognized blood group system at the time. The field has continued to move quickly since then. In September 2026, the International Society of Blood Transfusion announced JAMA as the 49th blood group system, illustrating how the genetic map of human blood is still being expanded.

Why the Discovery Matters for Transfusions

Knowing the gene behind AnWj gives blood specialists something they did not previously have: a direct genetic way to search for people who inherit AnWj-negative blood.

Genotyping tests can now be designed to identify rare patients and donors carrying the relevant MAL changes. These tests can potentially be incorporated into existing blood group genotyping systems.

That matters because finding compatible blood for someone with an antibody against a marker present in more than 99.9% of people can be extraordinarily difficult.

The need is not merely theoretical. Earlier clinical reports have shown that anti-AnWj antibodies can cause hemolytic transfusion reactions, in which transfused red blood cells are destroyed by the recipient’s immune system.

More recent cases have underscored just how complicated the situation can become.

In 2026, researchers reported a 75-year-old man with severe anemia and an anti-AnWj autoantibody. Compatible blood was unavailable, so physicians ultimately transfused unmatched red blood cells after weighing the risks. Genetic testing showed that his MAL gene was normal, supporting the conclusion that his antibody was acquired rather than caused by the rare inherited MAL deficiency. He did not experience a hemolytic transfusion reaction in that case.

Another 2026 case involved a patient with high-grade B-cell lymphoma and a complement-binding anti-ANWj autoantibody. After incompatible transfusions were followed by signs of red blood cell destruction, clinicians used sutimlimab, a drug that blocks part of the immune complement pathway. The patient’s laboratory measurements improved, although the researchers stressed that the complicated case and short treatment period prevent firm conclusions about the treatment’s effectiveness. It was reported as the first use of sutimlimab for this particular type of anti-AnWj-associated hemolysis.

Together, these cases highlight an important distinction. Some people are AnWj negative because of inherited MAL changes, while others can lose AnWj expression because of disease and develop an antibody against a marker their cells previously carried.

A Mystery That Took Decades to Crack

Louise Tilley, Senior Research Scientist, IBGRL Red Cell Reference at NHS Blood and Transplant, said: “The genetic background of AnWj has been a mystery for more than 50 years, and one which I personally have been trying to resolve for almost 20 years of my career. It represents a huge achievement, and the culmination of a long team effort, to finally establish this new blood group system and be able to offer the best care to rare, but important, patients.

“The work was difficult because the genetic cases are very rare. We would not have achieved this without exome sequencing, as the gene we identified wasn’t an obvious candidate and little is known about Mal protein in red cells. Proving our findings was challenging, and we appreciate the help of all our collaborators, and the patients, without whom we would not have got to this point.”

One reason the mystery endured for so long was simply the rarity of inherited AnWj negative blood. With so few known cases, researchers had very little genetic material from affected people to compare.

The Mal protein itself also offered few obvious clues. It is a very small protein embedded in cell membranes and has been associated with processes involving membrane organization and cellular transport. Nothing immediately pointed to it as the carrier of a long mysterious red blood cell antigen.

Gene Editing Helped Confirm the Answer

Ash Toye, Professor of Cell Biology in the School of Biochemistry and Director of the NIHR Blood and Transplant Research Unit in red cell products at the University of Bristol, said: “It’s really exciting we were able use our ability to manipulate gene expression in the developing blood cells to help confirm the identity of the AnWj blood group, which has been an outstanding puzzle for half a century. This development will help identify these rare donors and help patients in the future.”

Manipulating gene expression allowed the researchers to test cause and effect rather than simply observe that a genetic variant happened to occur in AnWj negative people. By changing which genes cells expressed and then testing whether AnWj appeared, the scientists could build a much stronger case that MAL was the missing piece.

Nicole Thornton, Head of IBGRL Red Cell Reference at NHS Blood and Transplant, said: “Resolving the genetic basis for AnWj has been one of our most challenging projects.

“There is so much work that goes into proving that a gene does actually encode a blood group antigen, but it is what we are passionate about, making these discoveries for the benefit of rare patients around the world.

“Now genotyping tests can be designed to identify genetically AnWj-negative patients and donors. Such tests can be added to the existing genotyping platforms.”

The official ISBT blood group database now lists the reference MAL allele along with the null allele associated with the AnWj negative phenotype, turning what was once an unexplained serological curiosity into a genetically defined blood group system.

Human Blood Is Far More Complicated Than ABO

The MAL story also illustrates how much complexity is hidden behind the familiar letters A, B, AB and O.

Blood groups are defined by inherited differences in molecules on red blood cells. These differences often have little noticeable effect in everyday life. They become important when the immune system encounters red blood cells carrying an antigen it recognizes as foreign, particularly during transfusion or pregnancy.

That is why rare blood group research can have an outsized clinical impact despite involving very few people. If a patient has an antibody against an antigen carried by nearly everyone else, locating compatible donor blood can require specialized laboratories, rare donor registries and sometimes international cooperation.

Dr. Tim Satchwell, Senior Lecturer at UWE Bristol, who contributed to the study whilst a Research Fellow at the University of Bristol, said: “Mal is a very small protein with some interesting properties which made it difficult to identify and meant we needed to pursue multiple lines of investigation to accumulate the proof we needed to establish this blood group system. Being able to combine our expertise to finally achieve this has brought the whole team a lot of satisfaction.”

For more than 50 years, AnWj was a blood antigen without a known genetic home. The identification of MAL changed that, giving researchers a molecular explanation, clinicians a path toward better genetic testing, and rare patients a better chance of being identified before a difficult transfusion becomes an emergency.

Notes

• Blood groups are complex. The two best known blood group systems are ABO and Rh. Within each blood group, red cells can carry surface markers called antigens. For example, within the ABO blood group system, there are the A and B antigens – people with A have the A antigen, people with B have the B antigen, people with AB blood have both and people with O have neither. There are now 47 recognized blood group systems together containing more than 360 recognized blood antigens.
• AnWj is named after the first people who made the antibody (Anton and Wj).
• The disorders suppress Mal and make patients AnWj-negative, unless they have the rare inherited form (MAL deletion). The inherited AnWj-negative people are healthy.

New research published in Science Translational Medicine focuses on primary aldosteronism, a hormone disorder that may affect up to one in five people with high blood pressure. The condition is associated with an increased risk of heart disease, stroke, diabetes, and other serious health problems.

Researchers from the University of Bristol and the University of Manchester in the UK, the University of Bergen in Norway, and collaborators in Stockholm and Athens found that people with primary aldosteronism can experience bursts of hormone production both during the day and while asleep at night. Those nighttime surges are especially important because routine blood tests are rarely performed during sleep.

A Wearable Device Tracks Hormones Around the Clock

To capture these hidden changes, the research team used a portable device developed at the University of Bristol that allowed patients to have their hormone levels monitored continuously while living normally at home rather than staying in a hospital or research facility.

This type of continuous monitoring could reveal abnormalities that may be missed by conventional testing, potentially helping doctors identify hormone-related conditions earlier.

Study co-lead author Dr. Thomas Upton, Clinical Research Fellow in Automated Sampling Clinical Fellow at the University of Bristol, and Senior Clinical Fellow at Bristol Hospitals NHS Foundation Trust said: “Primary aldosteronism is an important cause of high blood pressure and the most common cause of secondary hypertension we see in our blood pressure clinic. It could be affecting millions of people in the UK. However, due to the way hormones change during the day and the current complexity of the diagnostic process, diagnosis is often delayed or never made at all.

“In our study, patients were monitored at home during normal activity, and this allowed us to see how hormones changed over time in realistic settings. This approach could potentially revolutionize how we diagnose hypertension and ultimately reduce cardiovascular disease – particularly heart disease and strokes – that could have been prevented.”

Measuring Hormones Every 20 Minutes

The proof-of-concept study followed 60 patients in Bristol, Bergen, Stockholm, and Athens over a 24-hour period. Hormone levels were measured every 20 minutes using a lightweight wearable device about the size of a mobile phone that attaches at the waist.

Because the device samples hormones from the skin, participants were able to continue with their usual activities, including sleeping at night, while researchers collected detailed hormone data.

The technology, known as U-RHYTHM, was adopted and further developed by the spinout company Dynamic Therapeutics in 2023.

Study senior author Dr. Eder Zavala, UKRI Future Leader Fellow at the University of Manchester, said: “By continuously monitoring hormones over 24 hours, we were able to reveal a previously hidden pattern of nocturnal hormone bursts. This gives us a much clearer understanding of the disease and could ultimately help doctors detect it earlier and treat patients more effectively.

“A more detailed mathematical and computational analysis of daily hormonal profiles could eventually also help uncover earlier and more subtle forms of the disease, opening new opportunities to improve outcomes for patients living with high blood pressure.”

Why Standard Blood Tests May Miss the Disorder

Researchers used computational analysis to study changes in aldosterone, a hormone that helps control salt and water balance in the body. They also tracked two closely related hormones, 18-hydroxycortisol and 18-oxocortisol.

The results suggest that current diagnostic approaches may miss some patients because aldosterone does not remain consistently elevated.

Even in some of the most severe cases, hormone levels sometimes dropped below the minimum thresholds typically used to diagnose primary aldosteronism. A single blood test taken at one moment could therefore capture a period when hormone levels appear relatively normal.

Instead of remaining constantly high, aldosterone showed repeated bursts of secretion at night while the overall day-night rhythm of hormone activity remained intact.

Nighttime Hormone Bursts Offer a New Clue

The hormone spikes came from the adrenal glands and were especially pronounced in patients whose primary aldosteronism was caused by a problem affecting only one adrenal gland rather than both.

Importantly, the unusual hormone patterns disappeared after the affected adrenal gland was surgically removed. That finding provided additional evidence that the bursts were directly associated with the disease.

Study co-author Prof Stafford Lightman, Professor of Medicine at the University of Bristol and inventor of the U-RHYTHM technology, added: “The findings suggest that clinicians may need to rethink how they look for the disorder, which the Endocrine Society clinical practice guidelines now recommend should be considered for all people with hypertension, also known as high blood pressure.

“Future diagnosis could move away from single time point blood tests and towards tracking the body’s hormone rhythms over time, particularly the overnight patterns that appear to hold crucial clues to disease. Further research is needed to define the best clinical pathways, using dynamic hormone measurement, to ensure early diagnosis of this common and potentially curable cause of high blood pressure.”

Toward Earlier Detection of High Blood Pressure Causes

The findings raise the possibility that future testing for primary aldosteronism could rely less on a single blood sample and more on monitoring how hormones change over time.

Because the disorder can be treated and, in some cases, potentially cured, detecting it earlier could help reduce the risk of preventable cardiovascular complications.

The research was funded by EU Horizon 2020, the Trond Mohn Foundation, the UKRI Biotechnology and Biological Sciences Research Council (BBSRC), Medical Research Council, University Hospitals Bristol and Weston NHS Foundation, the Swedish Medical Research Council and Knut and Alice Wallenberg Foundation.

The findings support the University of Bristol’s research ‘Grand Challenge’ focus on Understanding and Preventing Cardiovascular Disease and builds on NIHR-funded initiatives aimed at earlier identification of people with hypertension and other cardiovascular risk factors.

This response is essential, but it is supposed to shut down once the danger has passed. As people age, however, certain cells accumulate that can keep inflammation active for much longer than necessary. This persistent inflammation has been associated with numerous diseases that become more common later in life.

Researchers at Sanford Burnham Prebys Medical Discovery Institute, Mayo Clinic, and collaborating institutions have now uncovered a previously unknown connection between mitochondria, cell metabolism, and this chronic inflammation. Their findings, published in Nature, also showed that interfering with part of the process reduced inflammation and supported healthier aging in mice.

How “Zombie” Cells Accumulate With Age

Many cells in the body are capable of dividing, allowing us to grow and helping tissues repair themselves after injury. But as we get older, increasing numbers of cells enter a state known as senescence. These zombie-like senescent cells stop dividing, yet they remain alive and active.

“Senescent cells are not completely inert,” said co-corresponding author Peter Adams, PhD, the Jeanne and Gary Herberger Leadership Chair in Cancer Research at Sanford Burnham Prebys. Adams also is director of and professor in the Cancer Genome and Epigenetics Program.

“They remain metabolically active and have an inflammatory program causing them to secrete inflammatory molecules.”

When senescent cells activate this inflammatory program, they are described as having the senescence-associated secretory phenotype (SASP). SASP has been linked to widespread inflammation associated with aging as well as a range of chronic diseases.

The research team, led by the laboratory of senior and co-corresponding author João Passos, PhD, a professor of Physiology at Mayo Clinic, set out to identify the molecular processes that drive SASP. Their broader goal was to determine whether those processes might be interrupted or reduced.

“It turns out that there is a convergence of at least two biological pathways related to mitochondria,” said Adams. “One alters how DNA is stored to promote areas related to SASP, and the other boosts the expression of the exposed SASP genes.”

Mitochondria Help Unlock Inflammatory Genes

Although senescent cells no longer divide, they continue using energy and carrying out metabolic activity. The researchers found that their mitochondria, the structures responsible for much of a cell’s energy production, behave differently from those in healthier cells.

In particular, mitochondria in senescent cells produced increased amounts of acetyl-CoA, an important molecule involved in metabolism.

Acetyl-CoA also interacts with histones, spool-like proteins around which DNA is wrapped. By altering these histones, acetyl-CoA can loosen the way DNA is packaged. This does not change the genetic code itself. Instead, it makes certain genes more accessible, including genes involved in the inflammatory SASP response.

That metabolic change alone, however, was not enough to explain why senescent cells continuously release inflammatory molecules.

Two Mitochondrial Signals Work Together

A second process was also required.

Damaged mitochondria can leak DNA and RNA into parts of the cell where those molecules normally should not be present. The immune system interprets this misplaced genetic material as a danger signal, triggering an inflammatory response.

These immune signals activate transcription factors that help switch genes on. Those factors are then able to target the SASP genes that have already been made more accessible by elevated acetyl-CoA.

In other words, the researchers found that two separate mitochondrial processes converge. One exposes inflammatory genes, while the other provides the immune signal needed to activate them.

“After seeing how these two independent pathways intersect, we wanted to see if interrupting one could prevent their partnership in promoting SASP,” said Adams.

Blocking the Metabolic Signal Reduced Inflammation

To test that possibility, the researchers used a drug called CTPI-2. The drug blocks a transport protein responsible for carrying a component needed to produce acetyl-CoA.

When CTPI-2 was tested in mice, it reduced inflammation throughout multiple tissues. The treatment also improved tissue function and healthspan during aging.

Importantly, the immune signals caused by leaking mitochondrial DNA and RNA were still present. But by weakening the metabolic signal involving acetyl-CoA, the researchers made SASP genes more difficult to access and reduced their inflammatory effects.

“Even though the immune signaling from leaky mitochondria was still present, disrupting the metabolic signal made SASP genes less accessible and produced functional benefits,” said Adams. “Using selective inhibitors such as CTPI-2 to reduce acetyl-CoA and, in turn, inflammation is a novel therapeutic strategy that should be explored.

“Also, more broadly, this research shows that targeting metabolic signals that influence DNA accessibility may represent a new approach for mitigating age-associated inflammation and functional decline.”

The findings suggest that changing the metabolic signals controlling access to inflammatory genes could offer a new strategy for addressing chronic inflammation and declining tissue function during aging.

Hélène Martini, PharmD, PhD, a postdoctoral researcher in the Passos lab at Mayo Clinic, is first author of the publication.

Additional authors include:

• Aaron Havas, Rabi Murad, Xue Lei and Rebecca A. Porritt at Sanford Burnham Prebys
• Anthony B. Lagnado, Nicholas Pirius, Ana Catarina Franco, Gung Lee, Yeaeun Han, Jennifer L. Rowsey, Stella Victorelli, Wazim Mohammed Ismail, Amelia Mazzone, Tianna M. Espe, Taro Hitosugi, Ya Li, Alexander M. Washington, Jair Machado Espindola-Netto, Dominik Saul, Sundeep Khosla, Diana Jurk, Enis Kostallari and Alexandre Gaspar-Maia at Mayo Clinic
• Jodie Birch at Imperial College London
• Francisco D. M. Marques at Albert Einstein College of Medicine
• Oliver D. K. Maddocks at the University of Glasgow

The study was supported by the National Institutes of Health, National Institute on Aging, National Cancer Institute, National Institute of Diabetes and Digestive and Kidney Diseases, Department of Defense Ovarian Cancer Research Program, Hevolution Foundation, The Glenn Foundation for Medical Research, Cancer Research UK, and Robert and Arlene Kogod Center on Aging.

Inflammation is one of the immune system’s most important defense responses. It helps the body fight infection and repair damaged tissue. But if that response remains active for too long, it can begin to harm healthy tissue and contribute to conditions including arthritis, heart disease, and diabetes.

Scientists have long known a great deal about how inflammation begins. What has been less clear is how the body decides that the danger has passed and shifts from fighting a threat to repairing the damage.

A Natural Brake on the Immune System

The new study, published in Nature Communications, points to a group of small fat-derived molecules called epoxy-oxylipins as part of that shutdown process.

According to the researchers, these molecules act like natural brakes on the immune system. They help prevent excessive growth of intermediate monocytes,* a type of white blood cell that can support healing in the short term but may contribute to chronic inflammation if too many accumulate or remain active for too long.

To study the process directly in people, the researchers gave healthy volunteers a tiny injection of UV-killed E. coli bacteria in the forearm. Because the bacteria were no longer alive, they could not cause an infection, but they still triggered a temporary inflammatory response.

That reaction produced the familiar signs of inflammation, including pain, redness, heat, and swelling, similar to what can happen after an injury or infection.

The volunteers were divided into two groups: prophylactic arm and therapeutic arm.

Researchers then gave participants a drug called GSK2256294 at different stages of the inflammatory response. The drug blocks an enzyme known as soluble epoxide hydrolase (sEH). Under normal conditions, sEH breaks down epoxy-oxylipins, so blocking the enzyme allows more of these protective molecules to remain in the body.

• Prophylactic arm: Participants received the drug two hours before inflammation began, allowing researchers to test whether increasing epoxy-oxylipins early could prevent harmful immune changes. In this group, there were 24 volunteers — 12 were treated, 12 untreated (placebo).
• Therapeutic arm: Participants received the drug four hours after inflammation started, better reflecting how a treatment might be used after symptoms have already appeared. In this group, there were 24 volunteers — 12 were treated, 12 untreated (placebo).

Pain Resolved Faster and Harmful Immune Cells Fell

Both approaches produced similar results.

Blocking sEH increased epoxy-oxylipin levels, helped pain resolve more quickly, and sharply reduced the number of intermediate monocytes found in both the blood and tissue. These immune cells have been linked to persistent inflammation and the progression of inflammatory disease.

The treatment did not, however, significantly change outward signs such as redness or swelling. That suggests the drug may have been altering deeper immune processes even when visible symptoms remained largely unchanged.

The researchers then investigated how the effect worked at the molecular level.

They found that one epoxy-oxylipin, 12,13-EpOME, appears to suppress a protein signaling pathway known as p38 MAPK. This pathway helps drive the transformation of monocytes into the intermediate form associated with prolonged inflammatory activity.

The team confirmed the mechanism in laboratory experiments and in volunteers who received a drug that directly blocks p38.

First author Dr. Olivia Bracken (UCL Department of Ageing, Rheumatology and Regenerative Medicine) said: “Our findings reveal a natural pathway that limits harmful immune cell expansion and helps calm inflammation more quickly.

“Targeting this mechanism could lead to safer treatments that restore immune balance without suppressing overall immunity. With chronic inflammation ranked as a major global health threat, this discovery opens a promising avenue for new therapies.”

A Possible Route to Safer Anti-Inflammatory Treatments

Many existing treatments for inflammatory and autoimmune diseases work by suppressing parts of the immune system. While that can reduce inflammation, it can also interfere with the body’s ability to defend itself.

The pathway identified in the new study may offer another strategy: strengthening a natural process the body already uses to bring inflammation under control.

Corresponding author Professor Derek Gilroy (UCL Division of Medicine) said: “This is the first study to map epoxy-oxylipin activity in humans during inflammation.

“By boosting these protective fat molecules, we could design safer treatments for diseases driven by chronic inflammation.”

He added: “This was an entirely human-based study with direct relevance to autoimmune diseases, as we used a drug already suitable for human use — one that could be repurposed to treat flares in chronic inflammatory conditions, an area currently bereft of effective therapies.”

Why Epoxy-Oxylipins Matter

Researchers focused on epoxy-oxylipins because earlier animal studies had suggested that these molecules can reduce inflammation and pain.

Their role in humans, however, had remained much less clear.

Compared with better-known inflammatory substances such as histamine and cytokines, epoxy-oxylipins belong to a relatively underexplored signaling system. Scientists suspected that this pathway might help the immune system naturally transition from an active inflammatory state toward recovery.

The new human study provides direct evidence supporting that idea.

Next Steps

The findings could pave the way for clinical trials testing sEH inhibitors in chronic inflammatory conditions, including rheumatoid arthritis and cardiovascular disease.

Dr. Bracken said: “For instance, rheumatoid arthritis is a condition in which the immune system attacks the cells that line your joints. sEH inhibitors could be trialed alongside existing medications to investigate if they can help prevent or slow down joint damage incurred by the condition.”

Rheumatoid arthritis is an autoimmune disease in which the immune system mistakenly attacks tissue around the joints, causing pain, swelling, stiffness, and potentially long-term damage.

Dr. Caroline Aylott, Head of Research Delivery at Arthritis UK, said: “The pain of arthritis can affect how we move, think, sleep and feel, along with our ability to spend time with loved ones. Pain is incredibly complex and is affected by many different factors. We also know that everybody’s pain is different.

“That is why it is important that we invest in research like this, that helps us understand what causes and influences people’s experience of pain.

“We are excited to see the results of this study, which has found a natural process that could stop inflammation and pain. We hope in the future that this will lead to new pain management options for people with arthritis.”

* Intermediate monocytes are white blood cells that help fight infection and repair tissue. In short bursts, they help coordinate the immune response and support recovery, but if they persist or grow in excess, they keep the immune system switched on, leading to chronic inflammation.

The study was funded by Arthritis UK and involved researchers at UCL, King’s College London, University of Oxford, Queen Mary University of London, and National Institute of Environmental Health Sciences, USA.