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Cellular mechanism represses immune reaction in type I-diabetes


According to a new study by researchers from Karolinska Institutet and University of Miami Miller School of Medicine, direct contact between different types of immune cells protects tissues from being attacked by the immune defence.

In type I diabetes, immune cells kill insulin-producing beta cells in the pancreas. It remains largely unknown how target tissue is damaged by immune cells, what protective mechanisms are in place and how tissue cells respond to inflammatory damage. In a new study, researchers at Karolinska Institutet and University of Miami Miller School of Medicine studied this by transplanting insulin-producing pancreatic cells into the mouse eye.

The study is the first to show that regulatory T helper cells in the target tissue have long-lasting direct contact with self antigen-directed killer T cells. The finding suggests that protective helper T cells may soften the aggressiveness of tissue-damaging T cells and control the immune reaction. The investigators also found that bystander tissue cells in the vicinity of attacked cells are not killed. Instead, they regenerate the damaged tissue by undergoing replication.

“This study shows that the tissue cells may not be mere ‘sitting ducks’ in a setting of autoimmune cell destruction. Rather, they may be capable of a resilient response at the inflammatory front,” says professor Per-Olof Berggren at the Rolf Luft Research Center for Diabetes and Endocrinology at Karolinska Institutet, one of the researchers behind the study.

The results suggest that insulin-producing beta cells can regenerate in the body by replication, resulting in a doubling in cell mass within days.

Source: Karolinska Institutet