A gene that can cause breast and ovarian cancer when mutated also seems to play a key role in T cell development, the soldiers of the immune system, according to a study this month of Nature Immunology . The results do not explain how the gene BRCA1 , contributes to cancer, but they shed new light on how T cells mature.
The mutations in BRCA1 were involved in about 5% of breast and ovarian cancer. Researchers believe that the BRCA1 gene normally plays a crucial role in DNA repair. Some suspected the gene may also be important in T cells - which fight bacterial infections, viruses and parasites - because these cells produce large amounts of the BRCA1 protein and because DNA repair is a natural part the trip of a T cell at maturity. To produce a wide variety of different T cells that can fight against any invader, the DNA encoding the receptor cells is remodeled during ripening, which means DNA strand must be broken and glued together.
for how significant BRCA1 is the immune system, a team led by molecular biologist Razqallah Hakim of the University of Toronto has created mice that lacked the protein in their cells T. As a result, they had 0% fewer cells than a control group T. their T cell population was also very young, suggesting that the cells had not completed their maturation process, and less sensitive to various stimuli. The scientists found that p53, a protein that responds to DNA damage or by halting cell division or causing the cell to commit suicide, was apparently involved in their disappearance. The knockout mice have high levels of p53 in the T cells, whereas the protein was undetectable in the control group.
But a follow-up experiment surprised researchers. It showed that T cells do not die as a result of the DNA shuffling that went wrong. After eliminating BRCA1 and also the gene p53 - thus preventing the cells from killing - the researchers found that animals produced normal amounts of T cells In addition, DNA sites where their receiver has been broken and repaired were intact.
Although BRCA1 be critical for the development of T cells, it may not be crucial for DNA repair in the redistribution of the receptor genes, said Doug Green, a researcher at the apoptosis in the la Jolla Institute for allergy and immunology in San Diego, California. "Most of us assume that this was the main source of DNA damage in these cells," he said. The next step, says Green, is to understand the role of BRCA1 in cancer development.
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