4.3. Th17 in atherosclerosis
Atherosclerosis (AS) is a chronic inflammatory disease of the
vasculature, which eventually leads to myocardial infarction or
stroke[53]. Current studies suggest that atherosclerosis results
from a complex interplay between innate and adaptive immunity. Th17
cells have both positive effects in promoting atherosclerotic plaque
stability and dual effects by secreting inflammatory factors or
promoting plaque growth[54]. On the one hand, clinical studies have
shown that, the production of pro-inflammatory cytokines IL-21 and
IL-22, which are involved in the accumulation of macrophages in the
arterial wall and the activation of T lymphocytes, can be induced by
Th17 cells. IL-17 promotes chemokine infiltration of inflammatory cells
into the arterial wall by upregulating adhesion molecules, including the
expression of intercellular adhesion molecules-1 (ICAM-1) together with
E-selectors. In addition, they enhance the inflammatory response by
inducing pro-inflammatory cytokines such as TNF-α and IL-6, to
participate in AS injury and enhancing the development of AS
lesions[55]. On the other hand, Th17 cells have been shown to reduce
the risk of subsequent myocardial infarction by promoting collagen
formation and thus preventing plaque rupture. In human atherosclerosis,
IL-17 co-evolves with the coronary plaque by infiltrating the IFN-γ via
T cells. On the top of this, IL-17 and IFN-γ collaboratively increase
the proinflammatory response through VSMCs, the levels of IL-17, IL-17A
were increased in human carotid AS plaque tissue, while the expression
of endothelial cell adhesion protein 1 was downregulated, smooth actin α
and collagenⅠwere significantly elevated, suggesting that IL-17 may
promote the stabilisation of AS plaque[56].