eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
Current issue Archive Manuscripts accepted About the journal Editorial board Abstracting and indexing Subscription Contact Instructions for authors Ethical standards and procedures
SCImago Journal & Country Rank
3/2021
vol. 46
 
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abstract:
Experimental immunology

Tim-1 alleviates lupus nephritis-induced podocyte injury via regulating autophagy

Yunxia Yu
1
,
Caixia Zhu
1
,
Nan Yu
1
,
Lijuan Yang
1

1.
Department of Rheumatology, the General Hospital of Ningxia Medical University, Yinchuan, Ningxia Province, China
Cent Eur J Immunol 2021; 46 (3): 305-313
Online publish date: 2021/10/19
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Introduction
Lupus nephritis (LN) is a complication of systemic lupus erythematosus (SLE) which seriously threatens the health of people. Tim-1 is known to be associated with the pathogenesis of SLE. However, the role of Tim-1 in LN is still unclear.
Aim of the study: To explore the expression and the potential regulatory molecular mechanism of Tim-1 in LN-induced podocyte injury.

Material and methods
An in vivo model of LN was established to detect the expression of Tim-1, inflammatory cytokines and autophagy-related proteins. Podocytes were treated with immunoglobulin G (IgG) to establish the LN in vitro model and then treated with an autophagy inhibitor. RT-qPCR and western blot were performed to investigate the effect of Tim-1 on inflammatory responses as well as autophagy in podocytes. The function of Tim-1 in IgG-induced podocytes was detected by CCK-8 and flow cytometry, respectively.

Results
Tim-1, L3BII/L3BI ratio and inflammatory cytokines were upregulated in LN mice. Tim-1 notably inhibited IgG-induced inflammatory responses in podocytes via reducing tumor necrosis factor  (TNF-), interleukin (IL)-6 and IL-1 expression, and it could protect podocytes against LN-induced injury via inducing autophagy. Meanwhile, Tim-1 significantly promoted the proliferation of IgG-induced podocytes via inhibiting apoptosis. The autophagy inhibitor reversed the effect of Tim-1 on inflammatory cytokines and autophagy-related proteins in IgG-treated podocytes.

Conclusions
Tim-1 protects podocytes against LN-induced injury via mediating autophagy, which might serve as a new target for the treatment of LN.

keywords:

lupus nephritis (LN), lupus nephritis, Tim-1, podocytes, autophagy

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