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Atherosclerosis-associated antigens are a heterogeneous group of molecules, including modified lipoproteins and stress-induced proteins, that drive the chronic inflammatory process within the arterial wall (Hansson & Hermansson, 2011, Nature Immunology). The most prominent antigens include oxidized low-density lipoprotein (oxLDL), heat shock proteins (HSP60/65), and apolipoprotein B-100 (ApoB-100), which are recognized by the innate and adaptive immune systems (Ketelhuth & Hansson, 2016, Circulation Research). These antigens facilitate the recruitment of macrophages and the activation of T-helper 1 (Th1) cells, leading to plaque formation and instability. Therapeutic interventions, such as atherovaccines or monoclonal antibodies, are designed to induce immune tolerance or neutralize these antigens to attenuate vascular inflammation (Grundtman et al., 2011, Arteriosclerosis, Thrombosis, and Vascular Biology). For instance, vaccines targeting ApoB-100 sequences aim to stimulate regulatory T cells that suppress the local inflammatory response in the vessel wall (Nilsson et al., 2013, Journal of Internal Medicine). Passive immunization strategies using monoclonal antibodies against oxLDL have also been explored to reduce lipid accumulation and inflammation. Despite their potential, the complexity of the immune response in atherosclerosis and the risk of cross-reactivity with non-target tissues remain significant hurdles for clinical application (Wolf & Ley, 2019, Nature Reviews Cardiology). Current research focuses on identifying specific epitopes that can provide long-term atheroprotection without compromising systemic immunity.
Induction of immune tolerance through regulatory T cell activation or neutralization of pro-inflammatory epitopes via passive or active immunization.
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