HOUSTON, SEPTEMBER 18, 2026 ― Researchers at The University of Texas MD Anderson Cancer Center have identified a previously unknown role for B cells, which are adaptive immune cells, in triggering and sustaining colitis occurring as a side effect of immune checkpoint inhibitors , a widely used form of cancer immunotherapy .
The study, published in Cell Reports , was led by Roza Nurieva, Ph.D. , professor of Immunology , together with co-first authors Naimah Turner, a research assistant in the Nurieva Laboratory; Synat Keam, Ph.D., postdoctoral fellow in the Nurieva Laboratory; Noha Abdel-Wahab, Ph.D., associate professor at Cleveland Clinic Ohio and Abu Dhabi, and additional collaborators. The findings suggest that changes in circulating B cell activity may occur before symptoms emerge, providing a potential blood-based biomarker to identify patients at risk of immunotherapy-related colitis.
"Immune checkpoint inhibitors have significantly improved outcomes for patients with advanced cancer, but they can also come with severe side effects that may disrupt treatment," Nurieva said. "Our study suggests that early B cell dysregulation sets off an inflammatory cascade in some patients while they are asymptomatic, serving as a driver of and predictive biomarker for risk of immunotherapy-related colitis that can guide future preventive treatment strategies."
What is immunotherapy-related colitis?
Immune checkpoint inhibitors have dramatically transformed the cancer treatment landscape, unleashing the immune system to recognize and eliminate cancer cells more effectively. However, these therapies can also trigger severe immune-related side effects in some patients, leading to a stop or pause in treatment.
Colitis is an inflammation of the inner lining of the colon and is among the most common side effects, causing severe diarrhea, abdominal pain and intestinal bleeding. Currently, there are limited tools to predict which patients will develop colitis before symptoms appear.
What did this study uncover about the role of B cells?
This study identified that higher levels of B cells prior to treatment were associated with an increased risk of immunotherapy-related colitis in patient samples. To confirm this association, the researchers developed preclinical models to mimic the inflammation seen in colitis, which allowed them to examine immune changes during the process. B cell activation occurred early on, preceding the expansion of inflammatory T cells that damage tissue and cause the inflammation that is characteristic of colitis.
Additionally, depleting B cells before treatment reduced signs of colitis and resulted in less intestinal damage and fewer inflammatory T cell responses, suggesting that B cells appear to initiate and amplify this cascade. B cells also help direct immune cell movement into the colon, reinforcing inflammation after it begins.
Does the gut microbiome play a role?
The researchers noted that preclinical models that were susceptible to colitis also had altered gut microbiomes associated with abnormal activation of B cells prior to receiving immunotherapy. Using fecal microbiota transplantation to restore healthy gut bacteria decreased the severity of colitis and reduced inflammation.
What does this mean for patients?
These preclinical results suggest that blood-based B cell measurements may help identify patients at higher risk of developing immunotherapy-related colitis before treatment begins. The results also suggest potential preventive approaches, such as targeting B cells or improving the gut microbiome. Further validation is needed in larger patient cohorts to confirm these findings.
