Figure 1. Theoretical events in initiation and effector phases of a proatherogenic T cell response.

Modified self-proteins generated in early atherosclerotic lesions (or systemically), such as the oxidatively modified apoB-100 component of LDL, are processed by DCs and presented as peptide/MHC complexes to naive T cells in secondary lymphoid tissues, leading to T cell clonal expansion and differentiation into effector T cells, such as Th1 or Th17 cells. The effector T cells migrate into arterial lesions, where resident macrophages or DCs present the same peptide-MHC antigens, leading to effector T cell activation and expression of pro-inflammatory effector molecules, such as secreted IFN-γ and IL-17 and membrane-bound CD40 ligand. These molecules promote lesion growth and/or destabilization.