Researchers discover antibody that can help kill cancer cells

New York: Researchers have found that an antibody — originally developed for studying the autoimmune condition multiple sclerosis — can promote the immune system's ability to fight cancer and decreases tumour growth.In a study published in the journal Science Immunology, the researchers reported that the antibody decreased tumour growth in models of melanoma (skin cancer), glioblastoma (brain cancer) and colorectal carcinoma, making it an attractive candidate for cancer immunotherapy.[caption id="attachment_2776844" align="alignleft" width="380"]

Representational imgae. Reuters[/caption]The antibody can precisely target regulatory T cells which in turn unleash the immune system to kill cancer cells.T cells (Tregs) which help maintain the immune system's tolerance of "self," can, inadvertently, promote cancer's growth by preventing the body's immune system from detecting and attacking cancer cells.The researchers, led by neurologist Howard Weiner from Brigham and Women's Hospital in Boston, Massachusetts, found that they could precisely target Tregs using an antibody.The team developed these so-called anti-LAP antibodies initially to investigate the development of multiple sclerosis, but realised their work had implications for the study of cancer.In the current study, the team used preclinical models to investigate how well anti-LAP antibodies could work in blocking the essential mechanisms of Tregs and restoring the immune system's ability to fight cancer.They found that anti-LAP acts on multiple cell populations to promote the immune system's ability to fight cancer, including increasing the activity of certain types of T cells and enhancing immune memory."In addition to studying its therapeutic effect, we wanted to characterise the mechanism by which the anti-LAP antibody can activate the immune system," said lead author Galina Gabriely, a scientist in the Weiner laboratory."We found that it affects multiple arms of the immune system," Gabriely said.