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Sunday, July 20, 2008 |
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Current issue
Training for hired killers
BY JOSEPH BONNER, KRISTINE KELLY & LYNN LOVE
Last February, Christian
Münz reported that natural
killer cells — the assassins of the body’s immune
system — go through a period of “training” in the
tonsils, lymph nodes and spleen before they are released into the
bloodstream. It’s during this period that immune system cells
called dendritic cells activate the natural killers in one of two
modes. Either the cells become full-fledged executioners or they
become dispatchers, secreting cytokines, a type of chemical
messenger protein that influences the strategies the body uses to
fight infection.
“We saw that dendritic cells were able
to make the natural killer cells proliferate, secrete cytokines,
and increase their killing ability,” Münz says.
“We then got curious about where this interaction takes
place.”
In the November 23 issue of Proceedings of the National Academy of Sciences, Münz and colleagues show that dendritic cells
and natural killer cells are found together in a specific area of
human lymph nodes. Two proteins that the dendritic cells secrete
ensure the survival and proliferation of the natural killer cells
and increase natural killer cell production of the protein
interferon-gamma.
It’s the interferon-gamma that’s
the key. Natural killer cells are part of the innate immune
response, broadly battling all types of infection. But
interferon-gamma signaling can sway the adaptive immune response,
which tailors its attack to a specific type of intruder. When they
interact with dendritic cells in the lymph nodes, the natural
killer cells become a bridge to the adaptive immune system, helping
direct its response.
“Our new findings change the view of
natural killer cells,” says Münz. “Initially it
was thought that as part of the innate immune response, they only
limit viral infection or tumor cell mass until the adaptive immune
response kicks in. Now we can see that natural killer cells
aren’t just effectors, but helper cells for the adaptive
immune response.”
January 28, 2005
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The Rockefeller University
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