Emerging Role of Dipeptidyl Peptidase-4 in Autoimmune Disease.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2022
Historique:
received: 07 12 2021
accepted: 14 02 2022
entrez: 21 3 2022
pubmed: 22 3 2022
medline: 3 5 2022
Statut: epublish

Résumé

Dipeptidyl-peptidase IV (DPP4), originally identified as an aminopeptidase in 1960s, is an ubiquitously expressed protease presented as either a membrane-bound or soluble form. DPP4 cleaves dipeptide off from the N-terminal of its substrates, altering the bioactivity of its substrates. Subsequent studies reveal that DPP4 is also involved in various cellular processes by directly binding to a number of ligands, including adenosine deaminase, CD45, fibronectin, plasminogen, and caveolin-1. In recent years, many novel functions of DPP4, such as promoting fibrosis and mediating virus entry, have been discovered. Due to its implication in fibrotic response and immunoregulation, increasing studies are focusing on the potential role of DPP4 in inflammatory disorders. As a moonlighting protein, DPP4 possesses multiple functions in different types of cells, including both enzymatic and non-enzymatic functions. However, most of the review articles on the role of DPP4 in autoimmune disease were focused on the association between DPP4 enzymatic inhibitors and the risk of autoimmune disease. An updated comprehensive summary of DPP4's immunoregulatory actions including both enzymatic dependent and independent functions is needed. In this article, we will review the recent advances of DPP4 in immune regulation and autoimmune rheumatic disease.

Identifiants

pubmed: 35309368
doi: 10.3389/fimmu.2022.830863
pmc: PMC8931313
doi:

Substances chimiques

Dipeptidyl-Peptidase IV Inhibitors 0
DPP4 protein, human EC 3.4.14.5
Dipeptidyl Peptidase 4 EC 3.4.14.5

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

830863

Informations de copyright

Copyright © 2022 Huang, Liu, Wei, Li, Gao, Dong, Rao and Zhong.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Jie Huang (J)

Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Xinxin Liu (X)

Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Yingying Wei (Y)

Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Xinlu Li (X)

Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Shupei Gao (S)

Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Lingli Dong (L)

Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Xiaoquan Rao (X)

Department of Cardiovascular Medicine, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

Jixin Zhong (J)

Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China.

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