Although it is known that B cells play a crucial role in both innate and adaptive immunity, the precise function they perform in anti-tumor immunity is still unknown. Scientists at Brigham and Women’s Hospital with skill in immunology teamed up with specialists in dermatology from Massachusetts General Hospital to additionally grasp the job of B cells and distinguish a subset of cells that might play a critical role. They used single-cell profiling, a method developed in collaboration with the Broad Institute, to examine these B cells in mouse and human cancers by examining all of the cell’s genes.
TIM-1, a cell surface receptor, was found to be present on these B cells as the melanoma developed. In addition, they characterized a number of the B cell’s immune-related accompanying cell surface proteins. Strangely, they tracked down that deleting a molecule TIM-1, yet no of the other going with proteins, decisively diminished cancer development. The researchers came to the conclusion that TIM-1 regulates B cell activation and the immune response against cancer, including the activation of another type of tumor-specific killer T cells to stop the growth of tumors.
“The collaboration across institutions was extremely fruitful as we combined our immunology expertise at the Brigham with work at David Fisher’s MGH laboratory where seminal discoveries in skin malignancies have been made,” said lead author Lloyd Bod, PhD, of the Department of Neurology at the Brigham, who conducted this work while completing his postdoctoral fellowship at the Brigham. Bod is now an Assistant Professor and an independent investigator at the Mass General Cancer Center. “The collaboration allowed us to test and demonstrate the therapeutic potential of targeting TIM-1 in melanoma models.”