Checkpoint Inhibitors Could Worsen Giant Cell Arteritis

According to a story from Healio, recent research has suggested that giant cell arteritis, a rare immune-mediated disease, could be made worse from the use of checkpoint inhibitors, a class of drug. Cornelia M. Weyand, MD, PhD, a professor of rheumatology at Stanford University, says that the mechanism of action in this illness likely involves both the innate immune system and adaptive immune system. The effects felt by the innate system result in the extravascular aspects of the illness, whereas the effects on the adaptive immune system trigger the characteristic vascular complications.

About Giant Cell Arteritis (GCA)

Giant cell arteritis, which is also called temporal arteritis, is a disease that causes inflammation of the large blood vessels. It is considered an autoimmune disease in which the immune system behaves abnormally and begins attacking healthy body tissue. Scientists still aren’t sure what triggers the immune reaction, but the varicella-zoster virus may play a role. The illness is associated with polymyalgia rheumatica in some cases. Symptoms of giant cell arteritis include vision problems or loss, vascular murmur (sound caused by abnormal blood flow), tinnitus, headache, pain in the tongue and jaw, headache, unusual scalp tenderness and sensitivity, and difficulty opening the mouth. Aortic dissection, which can be rapidly lethal, can occur in some cases. Because of this risk as well as the risk of permanent vision loss, giant cell arteritis is regarded as a medical emergency. A course of high-dose corticosteroids (usually prednisone) is administered as soon as possible. Tocilizumab is also used in some cases. To learn more about giant cell arteritis, click here.

Checkpoint Signaling

Patients with this disease, particularly if the aorta is affected, display signs of deficient checkpoint signaling, such as a reduction in the expression of PDL-1. In a mouse model of the disease, mice that were given an immune checkpoint inhibitor saw a major exacerbation of their inflammation. The researchers also noted that CD28 was found to have a positive impact on artery remodeling. 

With current treatments for the disease potentially carrying a risk of serious side effects (particularly with long-term use), these findings could put the scientific community on a path towards a new approach to treatment that could improve patient outcomes.

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