Once Upon a Time: The Adaptive Immune Response in Atherosclerosis—a Fairy Tale No More

Disease trends over time and CD4 + CCR5 + T-cells expansion predict carotid atherosclerosis development in patients with systemic lupus erythematosus

“…We also report that specific T cells subsets such as CD4 + CCR5 + T cells predict carotid atherosclerosis development in SLE patients. Activated T cell subset, play an important role in the pathogenesis of atherosclerosis [22,64] and comprise also circulating T follicular helper (Tfh)-like T cells, whose expansion has been previously suggested to reflect an abnormal interaction between T and B lymphocytes in patients with SLE [65], an event that might possibly contribute to accelerated atherosclerosis and enhanced risk of atherothrombosis [66,67] [68]. Longer follow up studies on larger patients cohorts, and more comprehensive study endpoints are required to verify the possibility that persistence of activated T cells subsets in the blood may be associated with (and possibly responsible of) detrimental vascular effects, which could be temporally unrelated with clinically detectable disease flares as indicated by the lack of association of T cells subsets with disease activity, vintage, steroids and immunosuppressant treatments as well as SLEDAI changes over follow-up (Supplemental Tables 5, 6a, 6b).…”

Genetic Depletion or Hyperresponsiveness of Natural Killer Cells Do Not Affect Atherosclerosis Development

“…Atherosclerosis is a chronic inflammatory disease characterized by accumulation of cholesterol, immune cells, and fibrous elements, forming atherosclerotic plaques in large and medium sized arteries 1 . Over the past 20 years, a large body of evidence supported the implication of innate and adaptive immunity in the development of the disease.…”

Deep sequencing of the T cell receptor β repertoire reveals signature patterns and clonal drift in atherosclerotic plaques and patients

“…However, T cells are a heterogeneous population and include many subsets which can either promote or suppress inflammation, posing significant challenges to declare the role and mechanism of T lymphocytes in the development of atherosclerosis. Some studies show that atherosclerosis is reduced in immunodeficient mice, and transferring CD4+T cells can reverse the atheroprotective effect of T cell defects [ 5 , 6 ], but studies on the CD4-deficient ApoE-/- mice observe the opposite effect [ 7 , 8 ]. Regardless of these complexity, a key point is that during the development of atherosclerosis, the activated/expanded T cells play functions, such as secreting inflammatory factors (IL-6, IL-1β and TNF-α), recruiting inflammatory cells and regulating inflammatory responses [ 9 ].…”