Acta Diabetologica

, Volume 55, Issue 5, pp 515–517 | Cite as

Soluble programmed death-1 ligand 1(sPD-L1) is significantly reduced in the serum of type 1 diabetes patients

  • Xiaohong Chen
  • Heming Guo
  • Sicheng Li
  • Cuiping Liu
  • Sisi Ding
  • Yun Huang
  • Chen Fang
  • Ji Hu
Short Communication


Type 1 diabetes (T1D) is an autoimmune disease resulting from destruction of insulin-producing β cells mediated by T cell activation. The balance of stimulatory and inhibitory signals provided by cell surface interactions between T lymphocytes and co-stimulatory molecules is crucial for maintaining peripheral immune tolerance. Excessive expression of positive molecules or negative molecular expression defects can induce T cell immune tolerance imbalance, leading to the occurrence of autoimmune diseases. Programmed death-1 (PD-1) and its ligand PD-L1, negative co-stimulatory signal, play an important role in the development and progression of T1D [1]. Soluble programmed death-1 ligand 1 (sPD-L1), thought to be released through proteolytic cleavage of membrane PD-L1, has little research in T1D. This study aimed to explore the presence of PD-L1 in serum of type 1 diabetes patients and to investigate the influential factors of sPD-L1.


Patients and serum samples

In this...



This study was funded by grants from the National Natural Science Foundation of China (Grant Number 81600607 to Chen Fang, and 81502865 to Yun Huang). This work was supported by the Open Research Project of Shanghai Key Laboratory of Diabetes Mellitus (SHKLD-KF-1604).

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

Ethical standard statement

All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the 1975 Declaration of Helsinki, as revised in 2008.

Human and animal rights

This article does not contain any studies with human or animal subjects performed by the any of the authors.

Informed consent

Informed consent was obtained from all patients for being included in the study.


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Copyright information

© Springer-Verlag Italia S.r.l., part of Springer Nature 2017

Authors and Affiliations

  1. 1.Department of Endocrinology, Second Affiliated HospitalSoochow UniversitySuzhouChina
  2. 2.Jiangsu Key Laboratory of Clinical ImmunologySoochow UniversitySuzhouChina

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