Role of soluble programmed death-1 (sPD-1) and sPD-ligand 1 in patients with cystic echinococcosis.

Abstract:

:The programmed death-1 (PD-1)/PD-ligand 1 (PD-L1) signaling pathway is a negative regulatory mechanism that inhibits T cell proliferation and cytokine production. Soluble PD-1 (sPD-1) and soluble PD-L1 (sPD-L1), are also involved in regulation of the PD-1/PD-L1 signaling pathway. In the present study, the expression levels of sPD-1 and sPD-L1, as well as those of T helper (Th)1 [including interleukin (IL)-2 and interferon gamma], Th2 (including IL-4, IL-6 and IL-10) and Th17 (including interleukin 17) cell cytokines, were measured in the sera of patients with cystic echinococcosis (CE). Measurements were performed prior to and following after surgery and treatment with cyclic albendazole to investigate the effects of sPD-1 and sPD-L1 in patients with CE. Cytokine expression levels were measured using cytokine bead array and the expression levels of sPD-1 and sPD-L1 were measured using ELISA. In addition, in vitro stimulation was used to detect whether sPD-L1 has a negative regulatory effect on cytokine secretion or homeostasis. The present study observed significantly higher levels of sPD-L1 in patients with CE compared with healthy controls. Significantly elevated levels of Th2 cytokines in the sera of patients with CE were also observed. The results also suggest that there is an imbalanced expression of Th1 and Th2 cells during CE. In addition, it was demonstrated that sPD-1 and sPD-L1 are regulatory factors to the PD-1/PD-L1 signaling pathway, each having opposite effect, suggesting that they regulate the immune response to CE infection by creating a dynamic balance. In conclusion, sPD-L1 may play an important role in maintaining homeostasis in hosts with CE.

journal_name

Exp Ther Med

authors

Li Y,Xiao Y,Su M,Zhang R,Ding J,Hao X,Ma Y

doi

10.3892/etm.2015.2876

subject

Has Abstract

pub_date

2016-01-01 00:00:00

pages

251-256

issue

1

eissn

1792-0981

issn

1792-1015

pii

ETM-0-0-2876

journal_volume

11

pub_type

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