September 5, 2019 — A research group at Johns Hopkins University discovered a new therapeutic mechanism that will help increase the efficacy of present immunotherapies and reduce the side effects in patients who are suffering from lung cancer. The analysis of this clinical study was published in The Journal of Clinical Investigation on September 4.
For patients with non-small cell lung cancer (NSCLC), evidence has given way for immunotherapies such as immune checkpoint inhibitors (ICI) can be an effective tool of treatment. ICI drugs block proteins, i.e. PD-1/PD-L1 & CTLA-4/B7-1/B7-2, made by a few types of immune cells and some cancer cells.
When these proteins are put to a block, they display an immune response that allows T cells to kill cancer cells.
However, activating the immune system can have irrelevant side effects. A dangerous predicament can be where up to 19% of patients develop checkpoint inhibitor pneumonitis (CIP), a complication caused by inflammation of the lungs.
Symptoms for this may include arthritis, colitis, endocrinopathies, and lung injuries. Patients with CIP have to stop cancer treatment at any cost. Despite the risk of CIP, ICI treatments are becoming the norm of care for the treatment of many kinds of cancers.
The research team at Johns Hopkins University ventured to study lung cells of NSCLC patients in order to analyze differences between patients with CIP and without. They also collected tissues from the lungs of 12 NSCLC patients with CIP and six patients being treated with ICIs who hadn’t really developed CIP. Samples were mostly collected through bronchoalveolar lavage (BAL).
This is the study first of its kind which is investigating the working of dysregulated alveolar immune dysregulation in people with CIP. “Based on the cell types we discovered, our study found various new pathways that could be investigated as therapeutic targets,” says Karthik Suresh, MD, co-author of the study.