This discovery, published in the Journal of Experimental Medicine, sheds new light on the role of the immune system in the development of type 1 diabetes. Normally, PD-L1 acts as a “stop signal” for immune cells, preventing them from attacking healthy tissue. But in these siblings, mutated PD-L1 rendered this function useless, leading to the destruction of insulin-producing beta cells in the pancreas that is the hallmark of type 1 diabetes.
The research team, collaborating with different institutions, discovered an unexpected development. Despite the critical role of PD-L1 in preventing type 1 diabetes, the patients’ overall immune system function appeared to be relatively normal. This suggests the existence of a backup system, possibly involving another protein called PD-L2.
Understanding the role of PD-L1 opens a new target for treatments that could prevent type 1 diabetes, explains Timothy Tree from King’s College London. This information may also benefit cancer immunotherapy, where manipulation of PD-L1 is currently being investigated.
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Source: Ferra
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