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Specialized White Blood Cells Prove Biomarkers for Diabetes Progression

By Labmedica International staff writers
Posted on 26 Aug 2019
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Image: Follicular helper T-cells (cells with green surface markers) interact closely with B-cells (cells with orange surface markers) to facilitate the proliferation of B- cells and the production of high affinity antibodies. The interaction site is shown in yellow, DNA in blue (Photo courtesy of Joyce Hu, La Jolla Institute for Allergy and Immunology).
Image: Follicular helper T-cells (cells with green surface markers) interact closely with B-cells (cells with orange surface markers) to facilitate the proliferation of B- cells and the production of high affinity antibodies. The interaction site is shown in yellow, DNA in blue (Photo courtesy of Joyce Hu, La Jolla Institute for Allergy and Immunology).
Researchers have found that a specialized class of circulating white blood cells (CXCR5−PD-1hi Tph cells) are associated with progression for autoantibody positivity to clinical type I diabetes and have the potential to serve as biomarkers to monitor progression of this disease.

Type I diabetes is preceded by a period of asymptomatic autoimmunity characterized by positivity for pancreatic islet autoantibodies. Therefore, T helper cell responses that induce B-cell activation are likely to play a critical role in the disease process.

To better understand the role of B-cell activation in type I diabetes, investigators at the University of Eastern Finland (Kuopio, Finland) aimed to evaluate the role of a recently described subset, C-X-C motif chemokine receptor type 5-negative, programmed cell death protein 1-positive (CXCR5−PD-1hi) peripheral T helper (Tph) cells, in human type I diabetes. C-X-C chemokine receptor type 5 (CXC-R5) is a G protein-coupled seven transmembrane receptor for chemokine CXCL13 (also known as BLC) and belongs to the CXC chemokine receptor family. It enables T-cells to migrate to lymph node B- cell zones.

Previous studies had found that the appearance of autoantibodies before clinical diabetes was caused by follicular helper T-cell activation of B-cells against proteins in the pancreatic islets. Peripheral helper T-cells (Tph) resemble follicular helper T-cells, but they express receptors that enable them to migrate to inflamed tissues.

For the current study, the investigators utilized samples from the Finnish DIPP (Type I Diabetes Prediction and Prevention) study in which the development of type I diabetes was followed from birth in children with genetic risk for the disease.

The frequencies of circulating CXCR5−PD-1hi T cells were analyzed by multicolor flow cytometry in a cohort of 44 children with newly diagnosed type I diabetes, 40 autoantibody-positive (AAb+) at-risk children, and 84 autoantibody-negative healthy control children. The findings were subsequently replicated in a separate cohort of 15 children with newly diagnosed type I diabetes and 15 healthy control children.

Results revealed that the frequency of circulating Tph cells was increased in children with newly diagnosed type I diabetes, especially in those who were positive for multiple autoantibodies. Importantly, circulating Tph cells were also increased in autoantibody-positive at-risk children who later progressed to type I diabetes.

"Based on our results, it is possible that peripheral helper T-cells may have a role in the development of type I diabetes. This information could be employed in the development of better methods to predict type I diabetes risk and new immunotherapies for the disease. However, more studies need to be conducted to verify our results and to further characterize the functionality of peripheral helper T- cells," said first author Ilse Ekman, a doctoral research student at the University of Eastern Finland.

The study was published in the September 2019 issue of the journal Diabetologia.

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University of Eastern Finland


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