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Naive CD4+ T cells differentiating into Apolipoprotein B (ApoB)-specific regulatory T cells (Tregs) represent a specialized immune pathway critical for cardiovascular health. These cells originate from naive precursors that recognize peptides derived from ApoB-100, the primary protein component of low-density lipoprotein (LDL), presented on MHC-II molecules (Wolf et al., Science 2022). Once differentiated, these ApoB-specific Tregs migrate to the arterial wall and lymphoid tissues where they exert immunosuppressive effects by secreting cytokines such as IL-10 and TGF-beta (Kimura et al., Circulation Research 2018). This activity inhibits the pro-inflammatory response of Th1 and Th17 cells, which are known to drive plaque formation. In atherosclerosis, this regulatory population is often diminished or dysfunctional, as chronic inflammation can trigger their conversion into "ex-Tregs" that promote rather than inhibit plaque progression (Ley, Nature Reviews Cardiology 2022). Therapeutic interventions, such as ApoB-peptide vaccines (e.g., p210), aim to expand this specific Treg population to restore immune tolerance and reduce vascular inflammation (Saigusa et al., Nature Reviews Cardiology 2020). Consequently, this differentiation process is a major focus for developing "atheroprotective" immunotherapies.
Induction of antigen-specific peripheral regulatory T cells (pTregs) from naive CD4+ T cells to suppress autoimmune-like responses against LDL components and reduce vascular inflammation.
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