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Researchers discover new signaling pathway for cell development

July 24, 2017

B-cells are lymphocytes that play a large role in immune responses and they make antibodies in response to infection or vaccination. They divide at the highest rate in the human body, faster than skin, hair or cells of the gastrointestinal tract. In making antibodies to fight infection or in response to a vaccine, these rapidly proliferating cells undergo DNA damage in order to make better, more effective antibodies. The body, in effect, is trading off the potential harm caused by added DNA damage in order to effectively ward off a more immediate invader.

The rapid cell cycling process that occurs during antibody assembly and testing by the immune system needs to be halted at the right time, Teitell said. The body naturally turns off that process after about two to three weeks. A defect in the new pathway interrupts that natural stop signal and blocks the production of effective antibody-producing cells, the plasma cells.

Mara Sherman, the first author of the study who worked as a graduate student in Teitell's lab, said the paper "reflects an exciting and emerging connection between DNA damage response pathways and cell differentiation."

"Our work points to this DNA damage-response pathway as a potential, novel therapeutic target for the treatment of B-cell lymphoma," Sherman said. "Combined with several intriguing recent studies, our work further suggests that pathways with established roles in genome maintenance may also drive the differentiation of stem and progenitor cell populations."

Patients at risk for developing B-cell related cancers could be screened for genes that, when not turned off, are a signature indicating pathway defects. The pathway also could be playing a role in the development of lung, colon and other major cancer types, Teitell said.

Going forward, Teitell and his team will further study the pathway to detail all aspects of its operation so new therapies can be developed to fix it when something goes wrong.

Source: University of California -- Los Angeles