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Long-Standing Puzzle Of Immune System Is Solved By UCSF Researchers

Researchers at the University of California San Francisco have solved a decades-long scientific puzzle about how the body's immune system works to combat illness.

In a study also having implications for better understanding cancer, the researchers found that the immune system is able to target virtually any unwanted microscopic invader within the body by subverting the function of an enzyme that normally is used to repair mistakes -- called mutations -- in the genetic material, DNA.

Immunology researchers have long suspected that immune cells take advantage of mutations that arise in genes to generate greater diversity in the genes that encode antibodies, proteins that mark disease agents for destruction. This diversity provides the immune system with a better selection from which to choose the best weapons for fighting disease.

Immunologists previously unearthed evidence indicating that immune cells can even activate mechanisms for producing additional mutations, a process dubbed hypermutation. But until now, none of the key molecular players used by immune cells to generate these mutations had been identified.

The study, co-authored by Mattias Wabl, PhD, professor of microbiology and immunology at UCSF and his laboratory team, is reported in the February 20 issue of Science.

"While mutations are, in general, harmful and unwanted, there is an important exception," Wabl explains. "B cells of the immune system depend on mutations in order to be ready to defend the body against newly arising pathogenic microorganisms.

"Without hypermutation at the immunoglobulin genes, which encode antibodies, we would likely have succumbed to an Andromeda strain long ago," Wabl says, referring to a popular science fiction thriller starring a newly arising microscopic scourge that threatens human life on Earth.

The cellular agent identified by the UCSF researchers as the one used by B c
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Contact: UCSF News Office
415-476-2557
University of California - San Francisco
20-Feb-1998


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