Intravital microscopy reveals details of key immune system process

Scientists at the University of Bonn (Germany), along with colleagues from the U.S. and Japan, used intravital microscopy to show how the body provides killer T-cells with helper T-cells during an infection. The study could someday lead to better vaccines.

Related: Intravital microscopy can study virus responses

If killer T-cells come upon a cell infected by viruses, they make holes in its cell membrane until the cell bursts and dies, preventing the virus from spreading further. The dendritic cells of the immune system collect evidence of an infection and hold it under the noses of the killer cells. The helper T-cells then boost the reproduction of killer T-cells and give them a helping hand.

In a lymph node, intravital microscopy photo shows the components of an important immune mechanism. The killer cells are shown in red, the helper cells are shown in blue, and connective tissue cells are shown in gray. The platform on which the killer and helper cells meet is stained green. (Source: Anna Brewitz/Kastenmueller laboratory)

Using intravital microscopy, the scientists discovered that killer and helper T-cells are initially separated from each other after an infection, in a state of alert. In this process, they are equipped with a type of GPS receiver: "This receiver guides the two to a so-called XCR1 cell," explains Prof. Dr. Wolfgang Kastenmueller from the University of Bonn. "That is a dendritic cell with special properties. Helper T-cells as well as killer T-cells can dock onto it."

(L-R) Prof. Dr. Wolfgang Kastenmueller, Anna Brewitz, Karl Komander, and Sarah Eickhoff. (Photo: Kathrin Kastenmueller/University of Bonn)

The microscopy technique enables cellular processes can be observed in living animals. The results may also be of interest for the development of new vaccines because killer cells are activated best by living viruses or bacteria. However, a live vaccine presents risks precisely in the case of harmful pathogens, which one would like to avoid. It would be better to be able to activate killer cells through harmless fragments of disease pathogens. "Over the long term, our findings could help turn this idea into reality," Kastenmueller says.

Full details of the work appear in the journal Cell; for more information, please visit

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