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.
Scientific Claim
In apolipoprotein E-knockout mice with induced vulnerable plaques, short-term combination stimulation increases the proportion of Th17 cells in splenocytes from 0.91% to 5.37% (p<0.001) at 14 weeks, while Th1 cell proportions remain unchanged, indicating a selective expansion of Th17 cells linked to plaque rupture.
Original Statement
“Although the proportion of Th17low cells was significantly increased in the treatment group compared with the control groups (6 weeks: 0.84%±0.26% vs 0.53%±0.17%, P<0.05 and 14 weeks: 5.37%±0.72% vs 0.91%±0.04%, P<0.001)... the proportion of Th1 cells did not differ significantly between the control and treatment groups both at 6 weeks and 14 weeks.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The study reports precise percentages and p-values from flow cytometry, showing a clear association without claiming causation. The language is precise and confined to the mouse model.
Evidence from Studies
Supporting (1)
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.