Scientists have identified a pro-inflammatory pair of genes – a receptor called CCR2 and its ligand CCL-2 – that work together to increase the risk of developing type 1 diabetes. Scientists say that this pair of genes recruits immune cells to the pancreas, which attack the insulin-producing islet cells, resulting in a lifelong course of insulin therapy and a lifelong increased risk of other health problems like heart and kidney disease
The study, published in the Journal of Translational Autoimmunity, provides evidence the CCR2 gene promotes progression to type 1 as it provides new insight on how to delay disease progression, says Paul Tran, MD/PhD student at MCG at Augusta University. Tran and Purohit are the study’s first authors.
The scientists were able to put the pieces together by looking at the longitudinal data on 310 people enrolled in DAISY, a National Institutes of Health-funded study based at the University of Colorado Anschutz Medical Campus in Aurora, that has been following individuals considered at risk for type 1 because of having a relative with it or having one of the genes associated with it since 1993.
The new study focused on 42 individuals who persistently had antibodies against the insulin-producing islet cells but never actually developed type 1, 48 who did develop type 1 and the remainder who did neither and served as the control group. They found that blood levels of CCL-2, the ligand for CCR2, were lower in both individuals who had antibodies but not actual disease as well as those who progressed to type 1 diabetes. They also found that both these groups have more of the receptors on their immune cells, which get recruited by the ligand to the six-inch organ in the abdomen that helps us break down the food we eat. Conversely, less receptors mean less recruitment of immune cells, more normal levels of CCL-2 in the blood and less cell destruction, they say.