#tregs

Winning Stroke

This study in a mouse model uncovers the molecular mechanisms underlying how exercise benefits recovery following a stroke. Cells of the immune system called regulatory T cells are found to be key – they're mobilised by exercise and their IL-10 molecular signalling pathway reduces neuronal hyperexcitability found in the stroke-affected region of the brain.

Read the published research article here

Image from work by A. Schmidt-Pogoda and colleagues

Department of Neurology, University of Münster, Münster, Germany

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, October 2025

Propaganda!

A chromosome is a package of DNA with part or all of the genetic material of an organism. In most chromosomes, the very long thin DNA fibers are coated with nucleosome-forming packaging proteins; in eukaryotic cells the most important of these proteins are the histones. These proteins, aided by chaperone proteins, bind to and condense the DNA molecule to maintain its integrity.[1][2] These chromosomes display a complex three-dimensional structure, which plays a significant role in transcriptional regulation.

Halting Diabetes Destruction

Type 1 diabetes occurs when the body’s immune system attacks its own pancreatic islet cells – specifically the beta cells, which produce insulin. The pancreatic islets of mice with a version of type 1 diabetes are shown above. On the left, the animal’s T cells can be seen crowding into the islet to destroy the beta cells, while on the right far fewer T cells are present. That’s because the animal on the right had been receiving daily injections of a recently discovered mitochondrial protein called MOTS-c, which possesses T cell regulatory activity. Animals treated with MOTS-c had preserved insulin production and improved blood glucose levels compared with controls. They also had significantly delayed onset of diabetes or no diabetes at all. The discovery that patients with type 1 diabetes have unusually low levels of MOTS-c suggests novel treatments aimed at boosting the protein’s activity may be of clinical benefit.

Written by Ruth Williams

Image from work by Byung Soo Kong and colleagues

Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea and Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Cell Reports, July 2021

Platelet One-eighty

An immune response to an infectious agent is all about balance. The initial blast of inflammation, as immune cells rush to kill the invader, must be cooled to stop excessive damage to the body’s own tissues. And new research indicates that platelets – small cell fragments that circulate in the blood – are central to both this surge and suppression of immune activity. Early in an infection, platelets (coloured red in this section of bacteria-infected mouse lung) are known to associate with inflammatory neutrophils to promote a strong attack. However, recent studies show that, later in infection, platelets form associations with anti-inflammatory regulatory T cells (Tregs, yellow). This alliance prompts the Tregs to produce signals that dampen the fire. Because failure to calm and resolve inflammation is a feature of many severe diseases, including COVID-19, understanding how platelets switch their allegiance to favour resolution could ultimately lead to therapies that promote it.

Written by Ruth Williams

Image from work by Jan Rossaint and colleagues

Department of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, Münster, Germany

Image copyright held by the original authors

Research published in Journal of Experimental Medicine, May 2021