Blog – Page 20

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.