Type 1 Diabetes

Type 1 Diabetes

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Type 1 Diabetes – The Davies Group

Type 1 Diabetes (T1D) is caused by immune cells that destroy the insulin-secreting cells in the pancreas. This results in uncontrolled high sugar (glucose) levels in the blood. T1D impacts about 5-10% of all those who have diabetes and usually develops in children and adolescents (https://www.cdc.gov/). In the days leading up to a diagnosis with T1D, people experience excessive thirst, vision change, fatigue, and weight loss. After diagnosis, people with T1D need to closely monitor their blood sugar levels and take insulin shots daily to stop their blood sugar levels from getting too high.

There is currently no cure for T1D, however San Diego BioMed scientists are looking at how the immune system prevents T1D in healthy people in an effort to potentially reverse the effects that lead to the disease.

The focus in the Davies research group is to understand how the immune system causes and prevents T1D. The research program is built on the premise that understanding how the immune system protects healthy individuals from T1D might shed light on pathways that can be targeted to reverse the immune defects that lead to the disease. This information might then be used to design strategies to rebuild the defective immune system so that the tissue is once again protected from immune-mediated damage. In the long term it is hoped that this program will contribute to our understanding and treatment of T1D.

Dr. Davies’ research program has identified a series of changes in the immune system that coincide with the onset of T1D. The group is now investigating whether these changes can be modified to reverse or reduce the severity of T1D and its complications.

Additionally, Dr. Davies’ group is investigating whether immune cell subset changes can identify which children are most likely to progress to diabetes and which will not. It is generally accepted that treating people early in the disease process is likely to be more beneficial than treating when diabetes is fully developed. The aim of this line of research is to identify children most likely to develop diabetes and then treat them before there is too much damage to the insulin secreting beta cells.

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Select Publications

Moya, R., Robertson, H.K., Payne, D., Narsale, A., Koziol, J., Type 1 Diabetes TrialNet Study Group, Davies, J.D. A pilot study showing associations between frequency of CD4+ memory cell subsets at diagnosis and duration of partial remission in type 1 diabetes. Clinical Immunology. 2016: 166:167-172.

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Zhao C, Marrero I, Narsale A, Moya R, Davies JD. CD4+ CD44v.low cells are unique peripheral precursors that are distinct from recent thymic emigrants and stem cell-like memory cells. Cellular Immunology. 2015; 296:106-114.

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Marrero I, Davies JD. High-throughput sequencing of islet-infiltrating memory CD4+ T cells reveals a similar pattern of TCR Vβ usage in prediabetic and diabetic NOD mice. PLoS One. 2013;8(10):e76546.

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Narsale A, Davies, JD. Memory T cells in Type 1 Diabetes: The Devil is in the Detail. Current Diabetes Reports. Curr Diab Rep. 2017 17:61-68.

Zhao C, Davies JD. A peripheral CD4+ T cell precursor for naïve, memory and regulatory T cells. J Exp Med. 2010;207(13):2883–94.

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Narsale A, Moya R, Davies JD. Human CD4+ CD25+ CD127hi cells and the Th1/Th2 phenotype. Clinical Immunology 2018 188:103-112

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El-Gohary Y, Tulachan S, Wiersch J, Guo P, Welsh C, Prasadan K, Paredes J, Shiota C, Xiao X, Wada Y, Diaz M, Gittes G. A smad signaling network regulates islet cell proliferation. Diabetes. 2014 63:224-36.

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Marrero I, Vong A, Dai Y, Davies JD. T cell populations in the pancreatic lymph node naturally and consistently expand and contract in NOD mice as disease progresses. Mol Immunol. 2012;52(i):9-18.

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Our research programs are funded primarily by grants from the National Institutes of Health (NIH). Private donations help to accelerate the progress of research through the purchase of laboratory supplies and equipment or the recruitment of additional laboratory personnel. Thank you!

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