ABSTRACT
Atherosclerosis is achronic arterial inflammatory process driven mainly by innate and adaptiveimmune mechanisms in response to modified lipoproteins. Genetically invalidated mouse models have identified several pathogenic T cell subsets implicated in atherogenesis. Th1 T cells that produce Interferon-γ accelerate atherosclerosis development and induce a “vulnerable” plaque phenotype [1]. Experimental studies examining the involvement of Th2 and Th17 T cells are contradictory, with some showing proatherogenic effects and others protective or no significant effect [2,
3]. In 2006, we have identified for the first time an atheroprotective T cell subset called regulatory T cells, that inhibits pro-atherogenic T cells [4] through several mechanisms, including the production of anti-atherogenic cytokines, such as IL-10 and TGF-β. Subsequently, several vaccination-like strategies have emerged to promote antigen-specific Treg cell responses with the aim of limiting atherosclerotic plaque development and/or vulnerability to rupture.
