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Jill de Mol

Immunologist at Leiden University who studies how the aging immune system, especially aged B cells, drives atherosclerosis, and first author of a 2026 study of rapamycin as an immune rejuvenator in old mice

Postdoc, Aging and Immunity group, Division of BioTherapeutics, LACDR, Leiden University · PhD candidate in Amanda Foks's group, Leiden University

Aging and Immunity group (Foks lab), Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University (Leiden, Netherlands) ↗ ORCID0000-0003-3541-9912 ↗

Atherosclerosis is the build-up of fatty, inflamed plaques in artery walls, and it gets worse with age partly because the immune system ages too. Jill de Mol is first author of a 2026 study from Amanda Foks's group in Leiden that gave rapamycin, which blocks the growth-control complex mTORC1, to old mice prone to atherosclerosis (JIN2026C). The plaques held fewer macrophages and T cells. Killer CD8 T cells shifted from an aggressive effector state to a calmer memory state, regulatory T cells that dampen inflammation increased in the aorta, and the antibody-making arm of immunity quietened, with fewer germinal-centre B cells, plasma cells and autoantibodies. Age-associated B cells dropped and the immune cells in the aorta looked less senescent, or worn out. The authors read this as rapamycin acting like an immune rejuvenation therapy. It is a mouse result; whether the same happens in older people is untested.

de Mol did a PhD in Foks's Aging and Immunity group at the Leiden Academic Centre for Drug Research and continues there as a postdoc. The group's work centres on aged B cell immunity in the plaque environment: the team found age-associated B cells in the blood and plaques of people with coronary artery disease and wants to understand them well enough to design targeted immune therapies for heart disease. In 2024 de Mol won a best poster award at the GEMSEQ meeting.

Milestones in the Atlas

A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.

YearEvidenceStudy
2026 A Therapeutic Immune Reprogramming by Rapamycin Attenuates Plaque Inflammation and Lymphoid Immune Responses in Aged Atherosclerotic Mice JIN2026C First author: showed in aged atherosclerotic mice that rapamycin reduced plaque inflammation and reset T and B cell responses toward a younger profile.

Co-authors in the Atlas 1

People with a profile here who share at least one study with Jill de Mol.

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  • Amanda C. Foks Studies how the immune system drives atherosclerosis and how it changes with age, including how rapamycin reshapes immune cells in aged atherosclerotic mice.

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