If it has seemed like more people you know are developing diabetes, you are right. The diabetes epidemic is not called an epidemic for nothing: According to the American Diabetes Association, over 10% of the U.S. population—approximately 38.4 million people—had diabetes in 2021, and 1.2 million more people get diagnosed each year.

Type 2 diabetes occurs when your body develops a resistance to insulin, the hormone that helps regulate glucose levels in your blood. Insulin is secreted by pancreatic cells called β-cells, and in T2D, they ramp up insulin production to try to regulate blood glucose levels, but even that is insufficient and the β-cells eventually become exhausted over time. Thanks to their importance, the functional β-cell mass, or the total number of β-cells and their function, determines a person’s risk of diabetes.

Β-cells are not homogeneous, even within a single individual, and consist of different “subtypes,” each with their own secretory function, viability, and ability to divide. In other words, each β-cell subtype has a different level of fitness, and the higher, the better. When diabetes develops, the proportions of some β-cell subtypes are changed. But a key question remains: Are the proportion and fitness of different β-cell subtypes altered by diabetes or are the changes responsible for the disease?

Weill Cornell Medicine researchers have discovered that PD-1—a molecule best known for putting the brakes on immune cells—also plays a critical role in helping T cells become long-term immune defenders in the skin. Early during infection, PD-1 acts like a steering wheel, guiding T cells to become protective resident memory T cells (TRM) that stay in place. These cells remember invading germs or cancer and quickly mount a response if that enemy reappears.

The preclinical findings, published July 29 in Nature Immunology, may impact how clinicians approach cancer treatments called immune checkpoint inhibitors. These drugs bind to PD-1 on the surface of T cells, releasing the brakes and unleashing the immune system to attack cancer cells.

Though immune checkpoint inhibitors are successful in treating melanoma, an aggressive skin cancer, about 40% of patients develop inflammatory rashes and itching in the skin or reactions in other epithelial tissues that cover internal and external surfaces of the body.

Background: Atherosclerosis is a progressive disease that results from endothelial dysfunction, inflammatory arterial wall disorder and the formation of the atheromatous plaque. This results in carotid artery stenosis and is responsible for atherothrombotic stroke and ischemic injury. Low-grade plaque inflammation determines biological stability and lesion progression. Methods: Sixty-seven cases with active perilesional inflammatory cell infiltrate were selected from a larger cohort of patients undergoing carotid endarterectomy. CD68+, iNOS2+ and Arg1+ macrophages and CD31+ endothelial cells were quantified around the atheroma lipid core using digital morphometry, and expression levels were correlated with determinants of instability: ulceration, thrombosis, plaque hemorrhage, calcification patterns and neovessel formation.

Patients with bronchial asthma suffer from attacks of shortness of breath caused by constricted airways. “Anti-inflammatory medications are usually given to treat this, although it isn’t quite clear how inflammation and constriction correlate,” says Professor Daniela Wenzel, head of the Department of Systems Physiology in the Faculty of Medicine at Ruhr University Bochum.

“These medications often stop working at a certain point.” Furthermore, asthma patients often experience a thickening of the bronchial tissue due to the accumulation of collagen. Goblet cells also form in increasing numbers, producing mucus and making breathing even more difficult. Currently, there is no medication to counteract these changes.