[Image via the NIH Image Gallery. Photo by Alex Ritter, Jennifer Lippincott Schwartz, and Gillian Griffiths. Full video, complete with narration here.]
Under the Radar: A series of listicles about biology concepts you definitely won’t find in newspaper headlines.
#1: Be a Navigation App for Immune Cells
Natural killer cells, or “NK cells” are the human body’s best defense against cancer. While other types of immune cells often ignore tumor cells, natural killer cells specialize in finding and destroying human cells that look either infected or like cancer mutants. In leukemia patients, a higher number of active natural killer cells ups the patient’s chances for survival, so much so that researchers are experimenting with transfusing NK cells into patients.
Just one problem there: Active natural killer cells die without a strong support network.
Dormant NK cells can survive in the bloodstream for a long time, but once activated, natural killers have to make a b-line for cells carrying a marker called IL-15 or die, but until a study in Monday’s edtion of PNAS , no one knew how natural killers knew to look for IL-15. The study, led by Vanderbilt immunologist Eric Sebzda and grad student Whitney Rabacal, traced NK cells’ IL-15 homing ability back to a biochemical with the horrendous name “Kruppel-like Factor 2” (KLF2).
KLF2, oddly enough, also exerts a strong navigational influence on the immune system’s T-cells and B-cells. Even though all three types of cells fall under the “white blood cell” umbrella, the notion that one protein could control navigation in all three is pretty weird. Crawling and navigating are complex tasks, requiring coordination between dozens of genes. “[NK cell migration] is totally different from how t-cells and b-cells circulate,” Sebzda said.
Additionally, taking away KLF2 has distinctive effects on each type of cell: KLF2-less t-cells vacate the central body and crawl out to lab mice’s fingers and toes, KLF2-less b-cells all congregate at the spleen (which creates some serious problems for those lab mice), and KLF2-less natural killers end up dying alone.
So KLF2 could be super-useful for improving cancer immunotherapy. But why is KLF2 so versatile in the first place?
The answer lies in KLF2’s ability to bind to a certain recurring DNA base pair sequence, one that presumably earmarks the genes needed in each immune system navigation system, and it’s far from the only protein with such abilities…
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