This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Immune cells are the elite athletes of the human body. While other cells stay in place, immune cells travel throughout our bodies, squeezing through small channels, stretching themselves, sampling the surfaces of other cells and swallowing up invaders.
One of their most extreme behaviors is NETosis, a process in which certain immune cells burst and release their DNA as a way to trap pathogens. NETosis, which is both critical when clearing infections and a liability in autoimmune diseases, involves several key steps: DNA, normally wound tightly into chromatin in the nucleus, unwinds itself; the nucleus breaks open to release DNA into the cell; the cell membrane ruptures, and the innards spill out. But the order of events and what triggers each step are poorly understood.
In a study published in Nature Communications, a team led by Hawa Racine Thiam, an assistant professor of bioengineering and institute scholar at Stanford University, discovered a key step in NETosis progression. They uncovered a previously unknown mechanism through which DNA, while stored inside the nucleus, puts stress on the cell membrane until it pops like an overfilled water balloon. The team also showed that they could leverage this mechanism to either prevent or speed up NETosis in cells.
By better understanding how cells rupture and identifying the levers that control key steps, scientists can develop new therapies for autoimmune diseases, cancer and more. "Immune cells teach us what is possible," said Thiam. "By studying extremes like NETosis, we are not just learning how immune cells behave, but we are also uncovering fundamental biology and learning what perhaps other cells are capable of.
And if we understand those behaviors, we can start to engineer those behaviors." Manasi Sawant, a postdoctoral scholar and co-lead author of the paper, has been studying what happens to chromatin inside the nucleus during NETosis. "Imagine a tangled ball of yarn. The thread of yarn is DNA, and it is twisted and molded into a tight space," said Sawant.
"During some processes, like NETosis, the chromatin decompacts, which means the DNA loosens up." Chromatin also unwinds itself at other times, like when healthy cells replicate themselves or when cancer cells mutate and become drug-resistant. By studying the steps by which chromatin unwinds during NETosis, Sawant hoped to learn more about these other processes, too. One way to study the unwinding is to look for the spools, the proteins that bind to DNA yarn and help keep it wrapped up tightly.
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