Israeli Scientists Uncover Immune Mechanism That May Hold the Key to Prolonging Healthy Human Life

By: Ariella Haviv

In a scientific breakthrough that researchers say could fundamentally reshape humanity’s understanding of aging, Prof. Alon Monsonego of Ben-Gurion University of the Negev has identified a population of immune cells that appear to decisively influence longevity. In an exclusive interview with The Times of Israel on Tuesday, Monsonego explained that his team’s discovery of a rare and potent subset of lymphocytes—cytotoxic T helper cells—may illuminate how the immune system governs the trajectory of aging itself.

The findings, recently published in Nature Aging, bring new clarity to one of biology’s most perplexing frontiers: why the body declines with time and what cellular systems may slow, halt, or even reverse aspects of that decline. Monsonego, a professor in Ben-Gurion’s Shraga Segal Department of Microbiology, Immunology and Genetics, emphasized that the research transcends the common preoccupation with lifespan. Instead, it focuses on “health span”—the number of years a person lives free of chronic disease, functional impairment, and degenerative decline.

“The immune system deteriorates with time, and that process may dictate the pace of aging,” Monsonego told The Times of Israel. “If we can understand how the immune system changes, and how certain cells function to prevent or slow those changes, we may uncover strategies to keep tissues healthier for much longer.”

At the core of Monsonego’s work is the phenomenon of cellular senescence, a process in which aging cells permanently stop dividing but do not die. These arrested cells accumulate steadily over decades, secreting inflammatory molecules that impair tissue function and drive major age-related diseases—from cancer to diabetes to heart disease.

Decades of research have framed senescent cells as silent saboteurs of biological integrity. Yet, according to Monsonego, it was not previously understood how the immune system targets or clears these toxic cells—or why its ability to do so degrades over time.

What his team has uncovered is that cytotoxic T helper cells, a distinctive category of lymphocytes previously not known to have this role, may function as the body’s natural cleanup crew, identifying and destroying senescent cells before they accumulate and cause damage.

“We found these cytotoxic T helper cells can be very effective in reducing the burden of senescent cells,” Monsonego explained. “This allows tissues to regenerate and recover.”

The discovery emerged partly by accident. When a Japanese research team published data showing that super-centenarians—people who live well past 100—have immune systems heavily populated with these rare cytotoxic T helper cells, Monsonego’s laboratory immediately recognized the pattern.

“It was a striking observation,” he told The Times of Israel. “These were the very cells we had been studying without yet understanding their full significance.”

Monsonego’s research into the immune system’s evolution over time began half a decade ago, when his team produced what he described as the first comprehensive “roadmap” of age-related changes in lymphocytes in mice.

“No one ever did that before,” he said. “We were pioneers in identifying, in detail, the dynamic changes of cytotoxic T helper cells in aging mice.”

The roadmap revealed an unexpected pattern: these T helper cells accumulated dramatically in aged mice, contradicting the conventional assumption that any cellular population increasing late in life must be harmful.

Initially, Monsonego admits, he thought the expansion was a sign that something was going wrong. “It surprised me. But science is full of surprises,” he told The Times of Israel. “The more we examined them, the more we saw that these cells were performing essential protective functions.”

To test their significance, the team genetically engineered mice lacking cytotoxic T helper cells. The result was unequivocal. “Without these cells, the mice lived shorter lives,” Monsonego said. “Their tissues deteriorated more rapidly. The consequences were clear.”

This convergence between murine data and findings from human super-centenarians has sent Monsonego’s research in a new direction: examining whether these exceptional long-lived individuals—particularly those in the world’s “Blue Zones”—possess uniquely robust populations of cytotoxic T helper cells.

Blue Zones, including Sardinia, Okinawa, Ikaria, and certain Jewish communities, have been widely studied for their unusually high concentrations of healthy elders. Monsonego believes their immune systems may offer invaluable insight into longevity’s biological architecture.

“Super-centenarians don’t just live long—they remain functional,” he said. “Our study suggests the immune system of healthy older individuals may have properties which we weren’t aware of before.”

However, Monsonego cautions against attributing longevity solely to genetics. “For most of us, it depends on how we live,” he said. “Increasing your lifespan means being aware that you need to work hard at it. Diet, exercise, and lifestyle matter enormously.”

Monsonego’s work aligns with a growing scientific emphasis on extending health span, not merely life span. He notes that degenerative conditions often begin as early as the early 40s—decades before outward signs of aging become apparent.

“When you say ‘aging,’ people think of their seventies,” he told The Times of Israel, “but it actually starts much earlier. If you want to preserve health span, you need to start early.”

The implications are far-reaching. Early identification of immune changes could pave the way for interventions that slow or prevent the onset of chronic disease long before symptoms appear.

“It’s not enough to live to 90 with five different diseases,” Monsonego emphasized. “We need to think about living healthy, not just living long.”

The publication of the Nature Aging study marks only the beginning of what Monsonego hopes will become a new field of research in biomedical science.

“We hope this research will lead to diagnostic tools and then therapy treatments to track and improve healthy aging,” he said.

According to Monsonego, the next steps include developing assays that can measure cytotoxic T helper cell function in individuals, creating therapeutic strategies to strengthen or replenish these cells, determining whether enhancing their activity can treat or prevent age-related diseases and understanding lifestyle factors that increase the abundance of these cells naturally.

“This is the long-term goal,” Monsonego told The Times of Israel. “To develop a diagnostic tool that can identify changes in T helper cells, and then, of course, to follow it with therapeutic strategies.”

Asya Rolls, professor of neuroscience at Tel Aviv University, who was not involved in the study, described Monsonego’s findings to The Times of Israel as “a transformative step in the biology of aging.”

“Aging might be more controllable than we thought,” she said. “Strengthening this natural immune mechanism could eventually open new ways to slow down age-related decline and keep tissues healthier for longer.”

Rolls added that the study presents one of the clearest biological bridges yet identified between immunity, inflammation, and longevity—fields long understood to be intertwined but not previously connected at this cellular level.

For decades, scientists have sought a unifying explanation for aging—a biological process that affects every organism yet remains profoundly mysterious. While no single discovery will reveal the entire picture, Monsonego’s work may provide one of its most crucial pieces.

By identifying the immune system’s natural anti-senescence mechanism, researchers may be edging closer to medically extending the body’s period of vitality—potentially transforming the last third of human life from a period of inevitable decline into one of continued health.

As Monsonego put it to The Times of Israel, “Medicine alone can’t do magic. But understanding how the immune system contributes to healthy aging may allow us to support that magic in ways we never imagined.”