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. Author manuscript; available in PMC: 2018 Sep 19.
Published in final edited form as: Circulation. 2017 Sep 19;136(12):1155–1166. doi: 10.1161/CIRCULATIONAHA.117.029870

Figure 2. Imbalance in adaptive immune pathways can modulate atherosclerotic plaque activity.

Figure 2

Subsets of T lymphocytes, major participants in adaptive immunity, can either promote local plaque inflammation (effector T cells), or, in the case of regulatory T cells (Treg) suppress inflammation. While many pathways regulate T cell functions, the markers and mechanisms depicted here illustrate the principle that imbalances in T cell activities can prevail in plaques. Low levels of expression of resurface marker CD 31 and high activity of PTPN22 (protein tyrosine phosphatase N22, also known as Lyp) characterize effector T cells. High levels of activation of CREB (cAMP-responsive element binding protein) characterize Treg that can dampen local adaptive immune responses in the plaque.