Researchers at Umeå University have shown in a new study that the environment in the womb can leave lasting imprints on the immune system and influence the risk of developing Type 1 diabetes, even when the genetic background is the same. The findings refine our understanding of how genetic and early environmental factors interact in autoimmune diseases.
“Our results from a mouse study suggest that the maternal immune system influences how the offspring’s immune cells mature and function, beyond what genetics alone can explain,” says Kristina Lejon, professor in the Department of Clinical Microbiology at Umeå University, who led the study.
The study, now published in Autoimmunity, is based on a well-established experimental model using mice that spontaneously develop Type 1 diabetes, known as NOD mice.
The researchers transferred NOD embryos into females of another mouse strain, B6. This approach allowed them to investigate how the fetal environment—independent of genetics—affects immune system development and the subsequent risk of disease.
NOD mice that developed in B6 females showed about a 50% lower incidence of Type 1 diabetes than NOD mice carried by NOD females. At the same time, the degree of inflammatory infiltration in the pancreas was comparable between the groups, suggesting that the difference lies in how the immune response is regulated rather than in whether inflammation occurs.
When the researchers examined the immune systems of these mice, they observed long-lasting changes. The immune system appeared more balanced, with an increased number of cells that dampen excessive immune responses and altered patterns of self-reactive antibodies.
This, in turn, may reduce the likelihood of disease development.
The researchers were able to rule out genetic differences and postnatal influences from the maternal gut microbiota as explanations for the effect.
“One possible explanation is instead that antibodies transferred via the placenta influence how the immune system is programmed early in life,” says Emma Renman, research engineer in the Department of Clinical Microbiology at Umeå University.
“This shows that maternal factors can shape the offspring’s immune system in a deeper way than previously understood,” says Lejon.
The study raises new questions about whether similar mechanisms may influence disease risk in humans and how early factors during pregnancy could potentially contribute to preventing autoimmune disease.
More information
Emma Renman et al, The in utero experience of NOD fetuses imprints disposition of B- and T-cell populations, autoantibody patterns, and diabetes development, Autoimmunity (2026). DOI: 10.1080/08916934.2026.2671674
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