Tuesday, October 25, 2022

High Blood Sugar Levels Trigger Immune Cell Activity that Drives MG: Study


According to a new study, the high blood sugar levels associated with diabetes may cause immune cells to become activated, which might fuel and exacerbate myasthenia gravis (MG).

These results suggest that patients with MG and diabetes may benefit from strict blood sugar control.

Published in Clinical Immunology, the study found that "Diabetes mellitus aggravates humoral immune response in myasthenia gravis by increasing differentiation and activation of circulating Tfh cells."

In MG, an autoimmune response prevents nerve and muscle cells from communicating with one another, leading to muscular weakness and other symptoms. Immune proteins known as antibodies, which are made by a class of immune cell known as B-cells, are what are driving this attack. The acetylcholine receptor is the target of the most prevalent type of MG-driving antibody (AChR).

November 4, 2021 News from PhD candidate Margarida Maia

Diabetes Could Trigger the Immune System in MG Patients, Worsening Symptoms

A metabolic condition called diabetes mellitus results in abnormally high levels of blood sugar or glucose. Diabetes may change immune system function, according to studies, but the implications for autoimmune illnesses like MG are unclear.

To investigate a potential link between diabetes and MG, researchers in China examined blood samples from 28 persons with MG—15 with diabetes and 13 without. In terms of age and gender distribution, both groups were comparable.

Researchers started by examining the quantities of circulating follicular helper T-cells (cTfh cells), an immune cell type that aids in the activation and antibody production of B-cells.

According to the findings, MG patients with diabetes exhibited larger concentrations of cTfh cells than those without. Additionally, cTfh cells in MG patients with diabetes produced higher activation markers, such as the protein ICOS.

In the current investigation, the researchers discovered that MG patients with [diabetes mellitus] had a greater number of cTfh cells. We then examined the activation markers of the cTfh cells and discovered that the cTfh cells of MG patients with [diabetes mellitus] expressed ICOS more frequently.

Next, researchers looked at B-cell counts. While the majority of B-cell populations in MG patients with and without diabetes were comparable, the data showed that diabetes was associated with significantly higher amounts of plasmablasts, B-cells that have been prepared to produce antibodies.

Statistical analysis revealed a substantial association between plasmablast levels and ICOS-expressing cTfh cell numbers.

Additionally, it was demonstrated through research in cell models that high glucose levels, such as those associated with diabetes, can encourage cTfh cell activation as evidenced by an increase in ICOS synthesis. These cTfh cells that were stimulated encouraged B-cells to develop into plasmablasts and manufacture antibodies. The results demonstrated that this glucose-driven cTfh cell activation was reliant on the action of a metabolic pathway known as mTOR.

The researchers concluded that diabetes and high glucose "appear to promote the generation of AChR-antibody secreting cells that drive MG" and that "the present results showed diabetes mellitus promoted cTfh cells differentiation and activation in MG patients, which positively correlated with increased plasmablasts in the blood." They claimed that MG patients with diabetes mellitus may benefit from "strict glycemic management."

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