When mice with fatty arteries were stressed, the number of a specific type of immune cell called Th17 went up dramatically — but another type, Th1, stayed the same, suggesting Th17 might be special in causing artery damage.

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Evidence from Studies

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Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

Cohort Study

Animal

2013 Jul

The study found that a specific stress combo in mice with bad artery plaques caused a spike in a type of immune cell (Th17) that makes inflammation, while other immune cells stayed the same—and this spike was tied to the plaques bursting.

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No contradicting evidence found

Source Study

Th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

Score: 17

DOI: 10.1038/cmi.2013.4

Similar Assertions

When the plaques burst in the mice, a chemical called IL-17 showed up in high amounts in their blood and right where the plaque broke — like a warning signal at the scene of the damage.

79%

After the plaque burst, the number of immune cells that calm down inflammation went up — like the body’s way of trying to fix the damage after the explosion.

74%

The cells that make both IL-17 and IFN-γ actually went down after stress — meaning the IL-17 causing damage probably came from cells that were already making it, not new ones being created.

73%

In the artery walls where plaques burst, the genes that make Th17 and Th1 immune cells were turned way up — showing the immune system was actively working right at the site of damage.

70%