Inhibitors of dipeptidyl peptidase 4, also DPP-4 inhibitors or gliptins, are a class of oral hypoglycemics that block DPP-4 (DPP-IV). They can be used to treat diabetes mellitus type 2.

Dipeptidyl peptidase-4 (DPP-4), also known as CD26, is the protease responsible for processing and inactivating both

DPP-4 is expressed on T lymphocytes, B lymphocytes and NK cells. Detailed studies of subsets of human CD4+ T helper cells show that DPP-4 expression is more restricted than most other immune accessory proteins, as DPP-4 is expressed only on CD4+ memory T helper cells, which induce immunoglobulin formation in B cells and activate cytotoxic T-cells. Furthermore, CD4+ T-cells lacking DPP-4 can respond to mitogens and alloantigens, but do not perform helper functions. DPP-4 co-stimulates both CD2 and CD3 dependent T-cell activation, and initiates a signaling pathway involving intracellular calcium mobilization. The co-stimulatory actions of DPP-4 include increased T-cell responses to foreign antigens, and initiation of signal transduction. This results in increased cytokine secretion and upregulation of T-cell activation markers (i.e. CD69, CD71 and CD25), resulting in the above mentioned helper functions for B cells and cytotoxic T-lymphocytes. The signal transduction pathway of DPP-4 outlined in T-cells overlaps with the T-cell receptor/CD3 pathway, increasing tyrosine phosphorylation of P56lck, p59fyn, ZAP-70, phospholipase C-y, MAPK and c-Cbl. Malignant cancer cells often show altered DPP-4 expression, where the DPP-4 present in these cells can act as both a tumor suppressor or activator. DPP-4 is also capable of binding to extracellular matrices, leading to increased invasive activity of the cells on which it is expressed.

Reference:Meghan Sauve. Genetic Elimination or Partial Selective Inhibition of DPP-4 Activity and Outcomes Following Experimental Ischemic Cardiac Injury in the Mouse

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