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'License to kill' enables powerful immune attack cells in mice

e Investigator and chief of the Division of Rheumatology at Barnes-Jewish Hospital. "Many of these terms refer to processes with a similar outcome--improved ability to distinguish between self and non-self--but this is a very different way of reaching that goal. So we came up with the term licensing."

Their results include another ironic connection to the world of cinema spies: the molecular details of the process feature a player who is comparable to a double agent. Scientists have known for some time that natural killer cells have inhibitory receptors on their surfaces.

The natural killer cells' ability to attack is inhibited when these receptors encounter a molecule known as major hiscompatibility complex (MHC) class I on the surface of other cells. MHC serves as a kind of molecular I.D. badge, helping the natural killer cells to distinguish the self from an invader.

But Yokoyama's group found that the inhibitory receptors switch roles during licensing. Although the structure of the receptors is exactly the same in immature natural killer cells, they act not as inhibitors but as enablers. In their studies, natural killer cells in mice became much more capable of mounting attacks against invaders after they first encountered the mouse version of MHC.

"The structure of these receptors on human natural killer cells is different from the mouse version, but they have a similar function," says lead author Sungjin Kim, Ph.D., research instructor in rheumatology. "We will be looking for a way to see if the human version also participates in some kind of licensing process."

The group's research was made possible by a unique mouse line created by Ted H. Hansen, Ph.D., professor of pathology and immunology and of genetics. Mice normally have many different versions of the MHC molecule, but Hansen created a line that makes only one. This was essential to the ability of Yokoyama's group to test its hypothesis.

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Source:Washington University School of Medicine


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