UCLA researchers discover how immune cells can be formed to fight viruses – NBC Los Angeles

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UCLA researchers have discovered the basic rule that allows immune cells in the human body to be trained to respond aggressively to viruses, bacteria and other invaders, the university said Thursday.

UCLA researchers have identified a molecular mechanism within macrophages, which are infection-fighting cells in the innate immune system, that determine whether and to what extent cells can be trained to fight invaders.

“Like a soldier or an athlete, innate immune cells can be trained by past experiences to become better at fighting infections,” said study lead author Quen Cheng, clinical assistant professor of diseases. infectious diseases at the Geffen School of Medicine at UCLA.

Cheng noted that some experiences seem to be better than others for immune training, and that “this surprising finding motivated us to better understand the rules that govern this process.”

The study was published in the journal “Science” on Friday, according to UCLA, which added that the findings could lead to strategies that improve immune system function.

According to the study’s lead author, Alexander Hoffman, professor of microbiology and director of the Institute for Quantitative and Computational Biosciences, researchers have found that immune entrainment can occur if a cell’s DNA is unwrapped. and exposes new genes that allow the cell to react more aggressively. When DNA is enveloped, only selected regions are exposed and accessible to fight infection.

UCLA researchers have found that the precise dynamics of a key immune signaling molecule in macrophages called NFKB, which helps immune cells identify threats, determine whether DNA is unwinding and whether genes are exposed. .

The researchers also reported that the dynamic activity of NFKB itself is determined by the precise type of extracellular stimulus introduced into macrophages.

“It is important to note that our study shows that innate immune cells can only be trained to become more aggressive by certain stimuli and not others,” said Cheng. “This specificity is essential for human health, as proper training is important to effectively fight infection, but improper training can lead to too much inflammation and autoimmunity, which can cause significant damage.”

NFKB is activated when receptors in immune cells sense threatening external stimuli. The dynamics of the NFKB form a language that UCLA researchers likened to Morse code – it communicates to DNA that there is an external threat and tells genes to prepare for battle.

The researchers used the bone marrow of mice to track NFKB activity in macrophages, according to UCLA. They tracked how the dynamics of the molecule changed in response to multiple stimuli. NFKB was only successful when the stimulus induced non-oscillating NFKB activity.

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“We’ve known intuitively for a long time that whether or not NFKB wobbles must be important, but we just haven’t been able to figure out how,” Cheng said. “These results are a real breakthrough in understanding the language of immune cells, and knowing the language will help us ‘hack’ the system to improve immune function. “

The training process was also simulated with a mathematical model, UCLA said. Mathematical modeling of immune regulatory systems is a key objective of Hoffman’s lab.

Hoffman and Cheng expect to inspire a wide range of other studies from their research, including investigations into diseases caused by immune cells, strategies for improving immune training to fight infections, and how to supplement them. existing vaccine approaches.

“This study shows how collaborations between researchers at UCLA College and the David Geffen School of Medicine can produce innovative and impactful science that benefits human health,” Hoffmann said. Cheng obtained his doctorate. under Hoffman’s direction at UCLA’s Specialized Training and Advanced Research Program.

The study’s co-lead author is Sho Ohta, assistant professor at the University of Tokyo and former postdoctoral researcher at Hoffmann’s UCLA lab. Co-authors also include UCLA MD and Ph.D. student Katherine Sheu; Roberto Spreafico, former postdoctoral researcher in Hoffmann’s laboratory; Adewunmi Adelaja, UCLA medical student who received his Ph.D. in Hoffmann’s laboratory; and Brooks Taylor, a former UCLA doctoral student in Hoffmann’s lab.

The study was funded by the STAR program of the Department of Medicine at UCLA and the National Institutes of Health.


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