Checkpoint inhibitors have revolutionized the care of patients with certain cancers; however, patients treated with these therapies often develop immune-related adverse events that strongly resemble rheumatic autoimmune diseases.
Rheumatologists are increasingly asked to treat these conditions with anti-inflammatory and immunosuppressive medications commonly used in rheumatic diseases. Pathogenesis of Checkpoint-Induced Arthritis on Monday, Nov. 9, from 4:15 – 5:15 p.m. will help rheumatologists understand some of the mechanisms that drive autoimmune-like conditions after checkpoint inhibitor therapy. The first viewing will offer a live question-and-answer period, but registered attendees have on-demand access to watch a replay of the session through Wednesday, March 11.
Current studies have set out to identify parallels with rheumatic diseases, as well as key differences, said Deepak Rao, MD, PhD, Assistant Professor of Medicine, Co-Director of the Human Immunology Center at Brigham and Women’s Hospital, Harvard Medical School. Dr. Rao has collaborated on this research with Hospital for Special Surgery (HSS) rheumatologists Drs. Anne Bass and Kimi Chan and HSS research scientist Laura Donlin, PhD, co-director of the HSS Precision Medicine laboratory and Assistant Professor at Weill Cornell Medicine, who will present during the session. Lukas Flatz, MD, of Kantonsspital St.Gallen, will also present.
“Understanding the pathways that mediate activation of anti-tumor responses and coinciding autoimmune-like reactions will help us better treat adverse immune effects of checkpoint blockade therapy,” Dr. Rao said.
Checkpoint inhibitors block breaks on immune cells, he said, unleashing immune reactions against tumors. Simultaneously, they activate undesired immune activation against multiple other tissues, most predominantly the gut, thyroid, lungs, skin, heart, and joints.
“To gain insights into the checkpoint-induced adverse events in the joint, we are comparing the immune responses in this condition to that seen in other diseases where we have more of an understanding, such as rheumatoid arthritis (RA) and psoriatic arthritis,” Dr. Rao said.
During the session, Dr. Donlin will describe the T cell phenotypes and functions that are prominent in joints of patients with checkpoint-induced arthritis and put these in the context of changes that are seen in RA and psoriatic arthritis. She will also highlight some of the key pathways activated in immune cells from checkpoint arthritis patients and the signals that activate these pathways.
Checkpoint inhibitor therapy has been an enormous advance in oncology, but has induced a new type of autoimmune-like diseases that researchers are only now starting to understand. These early studies are providing key insights into what goes on in checkpoint inhibitor-induced autoimmune conditions and how to establish the mechanisms involved in autoimmune-like rheumatic disease responses, Dr. Rao said.
“These studies may also help us gain new insights into how autoimmune rheumatic diseases are initiated,” he added.