B cells may help predict risk of colitis from immunotherapy
Researchers at The University of Texas MD Anderson Cancer Center have identified a previously unknown role for B cells, adaptive immune cells, in triggering and sustaining colitis as a side effect of immune checkpoint inhibitors, a widely used form of cancer immunotherapy.
Researchers at The University of Texas MD Anderson Cancer Center have discovered a new role for B cells, a type of immune cell, in triggering and perpetuating colitis—a side effect of immunotherapy treatments. The study, published in Cell Reports, suggests that changes in B cell activity may occur before symptoms of colitis appear, potentially serving as a blood-based biomarker to identify patients at risk.
Immune checkpoint inhibitors, a popular form of cancer treatment, can cause severe side effects like colitis, disrupting treatment regimens. The findings indicate that higher levels of B cells before treatment are linked to an increased risk of immunotherapy-related colitis in patient samples. The researchers' preclinical models revealed that B cell activation precedes the expansion of inflammatory T cells, which damage tissue and cause colitis.
Depleting B cells before treatment reduced colitis severity and intestinal damage, suggesting B cells initiate and amplify the inflammatory cascade. B cells also direct immune cell movement into the colon, exacerbating inflammation. Preclinical models with altered gut microbiomes, which are associated with abnormal B cell activation before immunotherapy, experienced reduced colitis severity and inflammation when their gut bacteria were restored through fecal microbiota transplantation.
These results imply that blood-based B cell measurements might help identify patients at higher risk of developing immunotherapy-related colitis before treatment begins, and that targeting B cells or improving the gut microbiome could be potential preventive strategies. Further validation in larger patient groups is necessary to confirm these findings.
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