Category: 8. Health

A new study published in Allergy from researchers at Sweden’s Karolinska Institutet reveals that biologic therapies mepolizumab and dupilumab—while clinically effective in reducing exacerbations and improving asthma control—do not fully eliminate type 2 inflammatory lymphocytes in individuals with severe asthma. Paradoxically, treatment is associated with increased frequencies of circulating type 2 innate lymphoid cells (ILC2), type 2 helper T cells (Th2), and cytotoxic T cells (Tc2), alongside phenotypic shifts that may alter their tissue homing and functional properties.

These findings suggest that persistent immune activation may continue under the surface, raising questions about the feasibility of biologic-free remission in some patients.

“We were surprised to find that blood levels of inflammatory cells increased rather than decreased,” Lorenz Wirth, doctoral student at Karolinska Institutet’s Department of Medicine in Huddinge, Sweden, said in a statement. “This could explain why inflammation of the airways often returns when the treatment is tapered or discontinued. It is important that we understand the long-term immunological effects of these drugs.”

The study addresses a critical gap in understanding how these targeted therapies influence immune cell dynamics beyond blood eosinophils. While biologics targeting interleukin (IL)-5 (eg, mepolizumab) or the IL-4 receptor alpha chain (eg, dupilumab) are now standard therapy for individuals with severe, eosinophilic, or Th2–high asthma, little is known about their impact on circulating type 2 lymphocytes—cells central to asthma pathogenesis. Given that some patients remain symptomatic despite treatment and that long-term remission is an emerging goal, researchers sought to characterize whether these cells persist or resolve with therapy.

Researchers analyzed peripheral blood samples from 40 participants with severe asthma enrolled in the longitudinal BIOCROSS study. All participants had uncontrolled asthma despite guideline-directed therapy and were treated with mepolizumab (n=33) or dupilumab (n=7). The research team collected blood samples at baseline, 4 months, and 12 months. Flow cytometry, single-cell RNA sequencing, and ex vivo stimulation assays were used to characterize type 2 lymphocyte populations and their transcriptional and functional changes over time.

FINDINGS

Clinically, both therapies led to significant improvements. Mepolizumab-treated participants showed reduced annual exacerbation rates (from 3.79 to 0.64; P <.001), decreased oral corticosteroid use, and improved Asthma Control Questionnaire (ACQ-6) and Asthma Quality of Life Questionnaire (AQLQ) scores. Participants treated with dupilumab also improved across similar measures, though the small sample size limited statistical comparisons, authors noted.

Yasinka and colleagues were surprised that, despite these gains, both treatments were associated with increased frequencies of circulating ILC2s. Mepolizumab also increased Th2 and Tc2 cells—particularly those with a central memory phenotype. These lymphocytes exhibited reduced expression of homing receptors, suggesting the potential for decreased airway trafficking, the researchers said. Notably, CD117^low ILC2s—associated with more active Th2 inflammation—were enriched in circulation, expressing elevated levels of CD62L and KLRG1.

Transcriptional analyses further revealed that mepolizumab-treated patients had increased expression of activator protein-1 (AP-1) family genes across type 2 lymphocyte subsets; the AP-1 family mediates biologic processes including proliferation and differentiation, authors explained. Functional assays supported these findings: after 1 year of treatment, type 2 lymphocytes produced more IL-5 and IL-13 in response to stimulation, indicating preserved or even enhanced pro-inflammatory potential despite biologic therapy.

The data put the paradox in context: while biologics reduce clinical symptoms and eosinophilic inflammation, they do not eliminate, and may even enrich, a population of functionally active type 2 lymphocytes with altered trafficking patterns. The authors hypothesize that mepolizumab, in particular, may redirect these cells away from inflamed airways into circulation—a mechanism that reduces local inflammation but does not equate to immune resolution.

Wirth et al acknowledge several limitations with the study, including the small size of the dupilumab subgroup and the absence of airway tissue samples. Findings are also limited to peripheral blood, which may not fully reflect activity in lung tissue, they wrote.

The authors conclude that long-term disease control in asthma may not equate to immunologic remission. Persistent inflammatory cell populations could represent a latent risk for disease flare or may influence decisions about tapering biologics, they advised. Further research should investigate whether specific biomarkers can identify patients likely to achieve durable, treatment-free remission or whether additional strategies are needed to suppress the full spectrum of type 2 inflammation.

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References

Wirth L, Weigel W, Stamper CT, et al. High-dimensional analysis of type 2 lymphocyte dynamics during mepolizumab or dupilumab treatment in severe asthma. Allergy. 2025;0:1–16 doi:10.1111/all.16633

Inflammatory cells remain in the blood after treatment of severe asthma. News release. Karolinska Institutet. June 26, 2025. Accessed July 2, 2025. https://news.ki.se/inflammatory-cells-remain-in-the-blood-after-treatment-of-severe-asthma

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All animal sales venues across Türkiye have been temporarily suspended as a precautionary measure to help control the spread of foot-and-mouth disease, Agriculture and Forestry Minister Ibrahim Yumaklı announced Tuesday.

“This decision is solely intended to speed up containment of the outbreak and is a temporary animal health measure,” he said.

In his statement regarding the outbreak, Yumaklı emphasized that the ministry continuously monitors and combats all diseases threatening animal health throughout the country.

“In 2024, thanks to our intensive vaccination campaigns and preventive measures against foot-and-mouth disease, we achieved an 80% reduction in cases compared to the previous year. Additional precautions were also taken during and before the Qurban Bayram, also known as Eid al-Adha, to manage animal movements,” he said.

Yumaklı reported that a new serotype of the disease (SAT1) was recently detected, and an effective vaccine was quickly developed and deployed by the ministry’s related departments. However, an increase in animal movement following the Eid holiday has caused a rise in SAT1 outbreaks, prompting the ministry to intensify vaccination efforts.

The minister stressed that vaccination alone is not sufficient to contain the disease. “Restricting animal movement is one of the most effective global standard practices in combating such diseases. Scientific assessments show that the risk of transmission is especially high in animal markets where direct contact occurs,” he said. Yumaklı also noted that indirect contact – through livestock traders, middlemen, and village visits – can spread the disease rapidly across regions. He emphasized that restricting animal movement at outbreak sites is crucial for both local and national animal health.

To support this approach, the minister shared the following updates: “To prevent the spread of foot-and-mouth disease and to ensure effective control, the activities of all animal markets, including livestock markets, live animal exchanges, animal collection and sales centers, fairs, and festivals, have been temporarily suspended. This is a preventive and short-term health measure. Vaccination efforts are continuing rapidly, and once the entire livestock population is vaccinated, the restrictions will be gradually lifted based on close monitoring of the outbreak.”

Yumaklı also reassured the public that the measures do not pose any threat to national food security, stating: “We do not expect any disruption in the supply of animal-based food products, especially meat and dairy. Our current stock and production infrastructure are sufficient to meet national demand. As the Ministry of Agriculture and Forestry, we are closely monitoring the situation, and our veterinary and field teams are on duty 24/7. In collaboration with all stakeholders, we are committed to eliminating threats to animal and public health.”

The minister concluded by reminding citizens that foot-and-mouth disease does not affect humans, and there is no risk in consuming red meat. He urged the public to follow official updates and guidance and thanked farmers and citizens for their awareness and cooperation.

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“The way we age as we get older is quite distinct from how many times we’ve traveled around the sun,” said Ahmad Hariri, professor of psychology and neuroscience at Duke University.

Now, scientists at Duke, Harvard and the University of Otago in New Zealand have developed a freely available tool that can tell how fast someone is aging, and while they’re still reasonably healthy — by looking at a snapshot of their brain.

From a single MRI brain scan, the tool can estimate your risk in midlife for chronic diseases that typically emerge decades later. That information could help motivate lifestyle and dietary changes that improve health.

In older people, the tool can predict whether someone will develop dementia or other age-related diseases years before symptoms appear, when they might have a better shot at slowing the course of disease.

“What’s really cool about this is that we’ve captured how fast people are aging using data collected in midlife,” Hariri said. “And it’s helping us predict diagnosis of dementia among people who are much older.”

The results were published July 1 in the journal Nature Aging.

Finding ways to slow age-related decline is key to helping people live healthier, longer lives. But first “we need to figure out how we can monitor aging in an accurate way,” Hariri said.

Several algorithms have been developed to measure how well a person is aging. But most of these “aging clocks” rely on data collected from people of different ages at a single point in time, rather than following the same individuals as they grow older, Hariri said.

“Things that look like faster aging may simply be because of differences in exposure” to things such as leaded gasoline or cigarette smoke that are specific to their generation, Hariri said.

The challenge, he added, is to come up with a measure of how fast the process is unfolding that isn’t confounded by environmental or historical factors unrelated to aging.

To do that, the researchers drew on data gathered from some 1,037 people who have been studied since birth as part of the Dunedin Study, named after the New Zealand city where they were born between 1972 and 1973.

Every few years, Dunedin Study researchers looked for changes in the participants’ blood pressure, body mass index, glucose and cholesterol levels, lung and kidney function and other measures — even gum recession and tooth decay.

They used the overall pattern of change across these health markers over nearly 20 years to generate a score for how fast each person was aging.

The new tool, named DunedinPACNI, was trained to estimate this rate of aging score using only information from a single brain MRI scan that was collected from 860 Dunedin Study participants when they were 45 years old.

Next the researchers used it to analyze brain scans in other datasets from people in the U.K., the U.S., Canada and Latin America.

Faster aging and higher dementia risk

Across data sets, they found that people who were aging faster by this measure performed worse on cognitive tests and showed faster shrinkage in the hippocampus, a brain region crucial for memory.

More soberingly, they were also more likely to experience cognitive decline in later years.

In one analysis, the researchers examined brain scans from 624 individuals ranging in age from 52 to 89 from a North American study of risk for Alzheimer’s disease.

Those who the tool deemed to be aging the fastest when they joined the study were 60% more likely to develop dementia in the years that followed. They also started to have memory and thinking problems sooner than those who were aging slower.

When the team first saw the results, “our jaws just dropped to the floor,” Hariri said.

Links between body and brain

The researchers also found that people whose DunedinPACNI scores indicated they were aging faster were more likely to suffer declining health overall, not just in their brain function.

People with faster aging scores were more frail and more likely to experience age-related health problems such as heart attacks, lung disease or strokes.

The fastest agers were 18% more likely to be diagnosed with a chronic disease within the next several years compared with people with average aging rates.

Even more alarming, they were also 40% more likely to die within that timeframe than those who were aging more slowly, the researchers found.

“The link between aging of the brain and body are pretty compelling,” Hariri said.

The correlations between aging speed and dementia were just as strong in other demographic and socioeconomic groups than the ones the model was trained on, including a sample of people from Latin America, as well as United Kingdom participants who were low-income or non-White.

“It seems to be capturing something that is reflected in all brains,” Hariri said.

The work is important because people worldwide are living longer. In the coming decades, the number of people over age 65 is expected to double, reaching nearly one fourth of the world’s population by 2050.

“But because we live longer lives, more people are unfortunately going to experience chronic age-related diseases, including dementia,” Hariri said.

Dementia’s economic burden is already huge. Research suggests that the global cost of Alzheimer’s care, for example, will grow from $1.33 trillion in 2020 to $9.12 trillion in 2050 — comparable or greater than the costs of diseases like lung disease or diabetes that affect more people.

Effective treatments for Alzheimer’s have proven elusive. Most approved drugs can help manage symptoms but fail to stop or reverse the disease.

One possible explanation for why drugs haven’t worked so far is they were started too late, when the Alzheimer’s proteins that build up in and around nerve cells have already done too much damage.

“Drugs can’t resurrect a dying brain,” Hariri said.

But in the future, the new tool could make it possible to identify people who may be on the way to Alzheimer’s sooner, and evaluate interventions to stop it — before brain damage becomes extensive, and without waiting decades for follow-up.

In addition to predicting our risk of dementia over time, the new clock will also help scientists better understand why people with certain risk factors, such as poor sleep or mental health conditions, age differently, said first author Ethan Whitman, who is working toward a Ph.D. in clinical psychology with Hariri and study co-authors Terrie Moffitt and Avshalom Caspi, also professors of psychology and neuroscience at Duke.

More research is needed to advance DunedinPACNI from a research tool to something that has practical applications in healthcare, Whitman added.

But in the meantime, the team hopes the tool will help researchers with access to brain MRI data measure aging rates in ways that aging clocks based on other biomarkers, such as blood tests, can’t.

“We really think of it as hopefully being a key new tool in forecasting and predicting risk for diseases, especially Alzheimer’s and related dementias, and also perhaps gaining a better foothold on progression of disease,” Hariri said.

The authors have filed a patent application for the work. This research was supported by the U.S. National Institute on Aging (R01AG049789, R01AG032282, R01AG073207), the UK Medical Research Council (MR/X021149/1), and the New Zealand Health Research Council (Program Grant 16-604).

A new artificial intelligence (AI) tool is helping doctors better understand and diagnose dementia, including Alzheimer’s disease, a new study has found. The tool, called StateViewer, was created by researchers at the Mayo Clinic. It was able to correctly identify the type of dementia a patient had in 88 per cent of cases, according to findings published in the journal Neurology.

Doctors say the tool could make it easier to diagnose dementia earlier, even in people who have other medical issues that make it hard to figure out the cause of memory loss or confusion.

“Every patient who walks into my clinic carries a unique story shaped by the brain’s complexity,” said Dr. David Jones, the study’s senior author and head of the Mayo Clinic’s Neurology AI Program. “StateViewer helps us give clearer answers, earlier.”

How does it work

To build the tool, researchers used over 3,600 brain scans called FDG-PET scans, which show how the brain uses sugar for energy. The AI compares a patient’s scan to a large database of scans from people with confirmed types of dementia.

It looks for patterns in brain activity linked to different types of dementia. For example:

• Alzheimer’s disease affects memory and thinking
• Lewy body dementia involves movement and attention
• Frontotemporal dementia affects language and behaviour

The AI can recognise patterns for nine different types of dementia, the researchers said.

StateViewer also creates colour-coded brain maps, making it easier for doctors to understand what the AI is seeing and why it gave a particular diagnosis.

“Behind every brain scan is a real person with a lot of questions,” said Leland Barnard, the lead researcher. “This tool gives doctors fast and accurate information that can help patients get the right care sooner.”

What’s next

The team now plans to test StateViewer in different hospitals and clinics to see how well it works in real-life situations.

If successful, it could become a useful tool for doctors treating people with memory problems or suspected dementia.

Experts say this is a step toward more precise, early diagnosis, which is important because treatment often works best when started early.

“This is just the beginning,” Dr. Jones said. “Tools like this could help change the way we care for people with dementia.”