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. Author manuscript; available in PMC: 2016 Apr 10.
Published in final edited form as: Circ Res. 2015 Apr 10;116(8):1491–1504. doi: 10.1161/CIRCRESAHA.116.305665

Figure 2. Mechanisms by which DPP4 modulates immune response of relevance to cardiovascular disease.

Figure 2

DPP4 regulates immune response via multiple mechanisms that involve both adaptive and innate immune function. These include: 1) Control of pericellular adenosine levels: adenosine triphosphate (ATP) or ADP is converted into AMP by membrane-bound CD39. AMP is further catalyzed by CD73 and produce adenosine. Adenosine is degraded by ADA bound to membrane-anchored DPP4. Accumulation of adenosine suppresses T cell activation and proliferation; 2) ADA-DPP4 interaction provides co-stimulatory signaling for T cell activation. By signaling through CD45, DPP4 enhances T cell receptor signals to promote T cell activation; 3) Inactivation of Glucagon-Like Peptide-1 (GLP-1). GLP-1 binds to GLP-1R and increases cAMP resulting in Protein Kinase A (PKA) mediated suppression of ERK, JNK, and NFκB; 4) Activation of APCs by interaction with caveolin-1. DPP4 binds to caveolin-1 and activates IRAK and NFκB, leading to the activation of APCs.