Negative immune regulatory molecule TIPE2 for treating SLE mice through regulating macrophage subtype
10.3969/j.issn.1671-8348.2017.24.002
- VernacularTitle:负向免疫调节分子TIPE2调控巨噬细胞亚型治疗狼疮小鼠的研究
- Author:
Xingjun LI
;
Yufen ZHANG
;
Feng LI
;
Xiaohua ZHU
;
Lan HUANG
- Keywords:
macrophages;
systemic lupus erythematosus;
adenoviridae;
ALD-DNA;
TIPE2
- From:
Chongqing Medicine
2017;46(24):3318-3320,3323
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of tumor necrosis factor (TNF)-alpha-induced protein 8-like 2 (TIPE2) for regulating the macrophage polarization in systemic lupus erythematosus and its curative effects on experimental SLE mice.Methods The mice were treated with activated lymphocytes derived DNA (ALD-DNA) for inducing mice model,randomly divided into AAV-scr control group and AAV-TIPE2 experimental group,and injected with AAV-TIPE2 or AAV-scr virus solution from the tail vein of mice.The expression of TIPE2 mRNA and protein in polarized macrophages,serum dsDNA antibody titer,urine protein and renal pathological index were detected.Results (1) The TIPE2 expression level of TIPE2 mRNA and protein in AAV-TIPE2-transfected cells was 13.5±1.6 times and 10.8±1.6 times of AAV-scr control group respectively.(2) M2 macrophage specific molecule MGL+ was 59.6% in AAV-TIPE2 group and MGL + cells in the AAV-scr group was 8.4%.M2/M1 odds ratio of AAV-TIPE2 experimental group to AAV-scr control group was 16.(3) The recombinant TIPE2 adenovirus related vector could stably expressed in transfected HEK-293.In vitro and in vivo experiments confirmed that AAV-TIPE2 was able to induce M2 polarization of macrophages in ALD-DNA-induced lupus mice.(4) The serum anti-dsDNA antibody,urinary protein and renal pathology in the AAV-TIPE2 group were significantly lower than those in the AAV-scr group(P<0.01).Conclusion TIPE2 alleviates the disease condition of ALD-DNA induced SLE mice through induction of macrophage polarization to M2 phenotype,which may be used as a promising therapeutic method for ALD-DNA induced SLE mice.
