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      Dipeptidyl peptidase 4 inhibitors and their potential immune modulatory functions

      review-article
      Author(s): a , a , a , b , a , *
      Publication date (Electronic):
      Journal: Pharmacology & Therapeutics
      Publisher: Pergamon Press
      Keywords: Dipeptidyl peptidase 4, Cluster of differentiation 26, Type 2 diabetes mellitus, Immunotherapy, AT, Adipose tissue, BP, Bullous pemphigoid, CVD, Cardiovascular disease, CCL, C-C motif chemokine ligand, CXCL, Chemokine (C-X-C motif) ligand, CPRD, Clinical Practice Research Datalink, CD26, Cluster of differentiation 26, CSF, Colony-stimulating factor, CD, Crohn's disease, CXCR4, CXC chemokine receptor 4, DC, Dendritic cell, DPP4, Dipeptidyl peptidase 4, DPP4is, DPP4 inhibitors, EPC, Endothelial progenitor cell, EPO, Erythropoietin, FGF2, Fibroblast growth factor 2, G-CSF, Granulocyte-CSF, GM-CSF, Granulocyte-macrophage-CSF, GLP-1, Glucagon like peptide-1, GIP, Glucose dependent insulinotropic peptide, HCC, Hepatocellular carcinoma, HFD, High fat diet, IBD, Inflammatory bowel disease, IFN-γ, Interferon gamma, IL, Interleukin, LADA, Latent autoimmune diabetes in adults, MI, Myocardial infarction, NK, Natural killer, NOD, Non-obese diabetic, OADs, Oral antidiabetic drugs, PCa, Prostate cancer, Treg, Regulatory T, RA, Rheumatoid arthritis, RASF, RA synovial fibroblast, SGLT2, Sodium glucose cotransporter 2, SGLT2i, SGLT2 inhibitor, sDPP4, Soluble DPP4, STZ, Streptozotocin, SDF-1, Stromal cell-derived factor-1, Th, T helper, TLR2, Toll-like receptor 2, TGF-β, Transforming growth factor-β, TNF-α, Tumor necrosis factor-α, T2DM, Type 2 diabetes mellitus, UC, Ulcerative colitis

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          Abstract

          Dipeptidyl peptidase 4 (DPP4) inhibitors (DPP4is) are oral anti-diabetic drugs (OADs) for the treatment of type 2 diabetes mellitus (T2DM) through inhibiting the degradation of incretin peptides. Numerous investigations have been focused on the effects of DPP4is on glucose homeostasis. However, there are limited evidences demonstrating their Potential modulatory functions in the immune system. DPP4, originally known as the lymphocyte cell surface protein CD26, is widely expressed in many types of immune cells including CD4(+) and CD8(+) T cells, B cells, NK cells, dendritic cells, and macrophages; and regulate the functions of these cells. In addition, DPP4 is capable of modulating plenty of cytokines, chemokines and peptide hormones. Accordingly, DPP4/CD26 is speculated to be involved in various immune/inflammatory diseases and DPP4is may become a new drug class applied in these diseases. This review focuses on the regulatory effects of DPP4is on immune functions and their possible underlying mechanisms. Further clinical studies will be necessitated to fully evaluate the administration of DPP4is in diabetic patients with or without immune diseases.

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          The lymphocyte chemoattractant SDF-1 is a ligand for LESTR/fusin and blocks HIV-1 entry.

          C. C. Bleul, M Farzan, H. Choe … (1996)
          Chemokines are chemotactic cytokines that activate and direct the migration of leukocytes. There are two subfamilies, the CXC and the CC chemokines. We recently found that the CXC-chemokine stromal cell-derived factor-1 (SDF-1) is a highly efficacious lymphocyte chemoattractant. Chemokines act on responsive leukocyte subsets through G-protein-coupled seven-transmembrane receptors, which are also used by distinct strains of HIV-1 as cofactors for viral entry. Laboratory-adapted and some T-cell-line-tropic (T-tropic) primary viruses use the orphan chemokine receptor LESTR/fusin (also known as fusin), whereas macrophage-tropic primary HIV-1 isolates use CCR-5 and CCR-3 (refs 7-11), which are receptors for known CC chemokines. Testing of potential receptors demonstrated that SDF-1 signalled through, and hence 'adopted', the orphan receptor LESTR, which we therefore designate CXC-chemokine receptor-4 (CXCR-4). SDF-1 induced an increase in intracellular free Ca2+ and chemotaxis in CXCR-4-transfected cells. Because SDF-1 is a biological ligand for the HIV-1 entry cofactor LESTR, we tested whether it inhibited HIV-1. SDF-1 inhibited infection by T-tropic HIV-1 of HeLa-CD4 cells, CXCR-4 transfectants, and peripheral blood mononuclear cells (PBMCs), but did not affect CCR-5-mediated infection by macrophage-tropic (M-tropic) and dual-tropic primary HIV-1.
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            Dipeptidyl-peptidase IV from bench to bedside: an update on structural properties, functions, and clinical aspects of the enzyme DPP IV.

            Anne-Marie Lambeir, Christine Durinx, Simon Scharpé … (2003)
            Dipeptidyl-peptidase IV/CD26 (DPP IV) is a cell-surface protease belonging to the prolyloligopeptidase family. It selectively removes the N-terminal dipeptide from peptides with proline or alanine in the second position. Apart from its catalytic activity, it interacts with several proteins, for instance, adenosine deaminase, the HIV gp120 protein, fibronectin, collagen, the chemokine receptor CXCR4, and the tyrosine phosphatase CD45. DPP IV is expressed on a specific set of T lymphocytes, where it is up-regulated after activation. It is also expressed in a variety of tissues, primarily on endothelial and epithelial cells. A soluble form is present in plasma and other body fluids. DPP IV has been proposed as a diagnostic or prognostic marker for various tumors, hematological malignancies, immunological, inflammatory, psychoneuroendocrine disorders, and viral infections. DPP IV truncates many bioactive peptides of medical importance. It plays a role in glucose homeostasis through proteolytic inactivation of the incretins. DPP IV inhibitors improve glucose tolerance and pancreatic islet cell function in animal models of type 2 diabetes and in diabetic patients. The role of DPP IV/ CD26 within the immune system is a combination of its exopeptidase activity and its interactions with different molecules. This enables DPP IV/CD26 to serve as a co-stimulatory molecule to influence T cell activity and to modulate chemotaxis. DPP IV is also implicated in HIV-1 entry, malignant transformation, and tumor invasion.
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              Efficacy and safety of incretin therapy in type 2 diabetes: systematic review and meta-analysis.

              Renee Amori, Joseph Lau, Anastassios G Pittas (2007)
              Pharmacotherapies that augment the incretin pathway have recently become available, but their role in the management of type 2 diabetes is not well defined. To assess the efficacy and safety of incretin-based therapy in adults with type 2 diabetes based on randomized controlled trials published in peer-reviewed journals or as abstracts. We searched MEDLINE (1966-May 20, 2007) and the Cochrane Central Register of Controlled Trials (second quarter, 2007) for English-language randomized controlled trials involving an incretin mimetic (glucagonlike peptide 1 [GLP-1] analogue) or enhancer (dipeptidyl peptidase 4 [DPP4] inhibitor). We also searched prescribing information, relevant Web sites, reference lists and citation sections of recovered articles, and abstracts presented at recent conferences. Randomized controlled trials were selected if they were at least 12 weeks in duration, compared incretin therapy with placebo or other diabetes medication, and reported hemoglobin A(1c) data in nonpregnant adults with type 2 diabetes. Two reviewers independently assessed trials for inclusion and extracted data. Differences were resolved by consensus. Meta-analyses were conducted for several efficacy and safety outcomes. Of 355 potentially relevant articles identified, 51 were retrieved for detailed evaluation and 29 met the inclusion criteria. Incretins lowered hemoglobin A(1c) compared with placebo (weighted mean difference, -0.97% [95% confidence interval {CI}, -1.13% to -0.81%] for GLP-1 analogues and -0.74% [95% CI, -0.85% to -0.62%] for DPP4 inhibitors) and were noninferior to other hypoglycemic agents. Glucagonlike peptide 1 analogues resulted in weight loss (1.4 kg and 4.8 kg vs placebo and insulin, respectively) while DPP4 inhibitors were weight neutral. Glucagonlike peptide 1 analogues had more gastrointestinal side effects (risk ratio, 2.9 [95% CI, 2.0-4.2] for nausea and 3.2 [95% CI, 2.5-4.4] for vomiting). Dipeptidyl peptidase 4 inhibitors had an increased risk of infection (risk ratio, 1.2 [95% CI, 1.0-1.4] for nasopharyngitis and 1.5 [95% CI, 1.0-2.2] for urinary tract infection) and headache (risk ratio, 1.4 [95% CI, 1.1-1.7]). All but 3 trials had a 30-week or shorter duration; thus, long-term efficacy and safety could not be evaluated. Incretin therapy offers an alternative option to currently available hypoglycemic agents for nonpregnant adults with type 2 diabetes, with modest efficacy and a favorable weight-change profile. Careful postmarketing surveillance for adverse effects, especially among the DPP4 inhibitors, and continued evaluation in longer-term studies and in clinical practice are required to determine the role of this new class among current pharmacotherapies for type 2 diabetes.
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                Author and article information

                Contributors
                Yong Chen
                Journal
                Journal ID (nlm-ta): Pharmacol Ther
                Journal ID (iso-abbrev): Pharmacol. Ther
                Title: Pharmacology & Therapeutics
                Publisher: Pergamon Press
                ISSN (Print): 0163-7258
                ISSN (Electronic): 1879-016X
                Publication date PMC-release: 14 February 2020
                Publication date (Electronic): 14 February 2020
                Electronic Location Identifier: 107503
                Affiliations
                [a ]Division of Endocrinology, Department of Internal Medicine, Tongji hospital, Tongji medical college, Huazhong University of Science & Technology, Wuhan 430030, PR China
                [b ]Department of Nuclear Medicine, Tongji hospital, Tongji medical college, Huazhong University of Science & Technology, Wuhan 430030, PR China
                Author notes
                [* ]Corresponding author at: Division of Endocrinology, Tongji Hospital, Huazhong University of Science & Technology, Jiefang Road 1095, Wuhan, Hubei Province 430030, PR China. tj.y.chen@ 123456vip.163.com
                Article
                Publisher ID: S0163-7258(20)30031-0 Publisher ID: 107503
                DOI: 10.1016/j.pharmthera.2020.107503
                PMC ID: 7102585
                PubMed ID: 32061923
                SO-VID: 1e35ee2f-bd39-4b56-afd8-871f82a4a320
                Copyright © © 2020 Elsevier Inc. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: dipeptidyl peptidase 4,cluster of differentiation 26,type 2 diabetes mellitus,immunotherapy,at, adipose tissue,bp, bullous pemphigoid,cvd, cardiovascular disease,ccl, c-c motif chemokine ligand,cxcl, chemokine (c-x-c motif) ligand,cprd, clinical practice research datalink,cd26, cluster of differentiation 26,csf, colony-stimulating factor,cd, crohn's disease,cxcr4, cxc chemokine receptor 4,dc, dendritic cell,dpp4, dipeptidyl peptidase 4,dpp4is, dpp4 inhibitors,epc, endothelial progenitor cell,epo, erythropoietin,fgf2, fibroblast growth factor 2,g-csf, granulocyte-csf,gm-csf, granulocyte-macrophage-csf,glp-1, glucagon like peptide-1,gip, glucose dependent insulinotropic peptide,hcc, hepatocellular carcinoma,hfd, high fat diet,ibd, inflammatory bowel disease,ifn-γ, interferon gamma,il, interleukin,lada, latent autoimmune diabetes in adults,mi, myocardial infarction,nk, natural killer,nod, non-obese diabetic,oads, oral antidiabetic drugs,pca, prostate cancer,treg, regulatory t,ra, rheumatoid arthritis,rasf, ra synovial fibroblast,sglt2, sodium glucose cotransporter 2,sglt2i, sglt2 inhibitor,sdpp4, soluble dpp4,stz, streptozotocin,sdf-1, stromal cell-derived factor-1,th, t helper,tlr2, toll-like receptor 2,tgf-β, transforming growth factor-β,tnf-α, tumor necrosis factor-α,t2dm, type 2 diabetes mellitus,uc, ulcerative colitis
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: dipeptidyl peptidase 4, cluster of differentiation 26, type 2 diabetes mellitus, immunotherapy, at, adipose tissue, bp, bullous pemphigoid, cvd, cardiovascular disease, ccl, c-c motif chemokine ligand, cxcl, chemokine (c-x-c motif) ligand, cprd, clinical practice research datalink, cd26, cluster of differentiation 26, csf, colony-stimulating factor, cd, crohn's disease, cxcr4, cxc chemokine receptor 4, dc, dendritic cell, dpp4, dipeptidyl peptidase 4, dpp4is, dpp4 inhibitors, epc, endothelial progenitor cell, epo, erythropoietin, fgf2, fibroblast growth factor 2, g-csf, granulocyte-csf, gm-csf, granulocyte-macrophage-csf, glp-1, glucagon like peptide-1, gip, glucose dependent insulinotropic peptide, hcc, hepatocellular carcinoma, hfd, high fat diet, ibd, inflammatory bowel disease, ifn-γ, interferon gamma, il, interleukin, lada, latent autoimmune diabetes in adults, mi, myocardial infarction, nk, natural killer, nod, non-obese diabetic, oads, oral antidiabetic drugs, pca, prostate cancer, treg, regulatory t, ra, rheumatoid arthritis, rasf, ra synovial fibroblast, sglt2, sodium glucose cotransporter 2, sglt2i, sglt2 inhibitor, sdpp4, soluble dpp4, stz, streptozotocin, sdf-1, stromal cell-derived factor-1, th, t helper, tlr2, toll-like receptor 2, tgf-β, transforming growth factor-β, tnf-α, tumor necrosis factor-α, t2dm, type 2 diabetes mellitus, uc, ulcerative colitis

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