EXPERIMENTAL RESEARCH
Effect of Toll-like receptor 4 deficiency on clinical severity and expression of Th1/Th2/Th17-associated cytokines in a murine model of experimental autoimmune neuritis
Li-Juan Wang 1,2,3,4
,
 
Jie Zhu 5,6
,
 
,
 
,
 
Chun-Jiao Yang 1,2,3,4
,
 
Xi-Xiong Kang 1,2,3,4
,
 
,
 
Guo-Jun Zhang 1,2,3,4
 
 
 
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1
Laboratory Diagnosis Center, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
2
China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
3
Monogenic Disease Research Center for Neurological Disorder, Beijing, China
4
Precision Medicine Research Center for Neurological Disorder, Beijing, China
5
Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden
6
Neuroscience Center, Department of Neurology, the First Hospital of Jilin University, Changchun, China
7
Department of Life Sciences, the National Natural Science Foundation of China, Beijing, China
Submission date: 2019-06-14
Final revision date: 2019-09-29
Acceptance date: 2019-10-14
Online publication date: 2020-05-07
 
 
KEYWORDS
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ABSTRACT
Introduction:
The aim was to observe the effect of Toll-like receptor 4 (TLR4) deficiency on clinical severity and expression of Th1/Th2/Th17-associated cytokines in experimental autoimmune neuritis (EAN).

Material and methods:
We selected C57BL/10 wild type (WT) mice and TLR4 knockout (KO) mice with the C57BL/10 background for induction of the EAN model by immunizing mice twice (days 0 and 8) via subcutaneous injection of 180 µg P0 peptide 180–199 emulsion in 25 µl of PBS and 0.5 mg Mycobacterium tuberculosis (Difco, USA) in 25 µl of Freund’s incomplete adjuvant into the back of mice. The concentrations of serum cytokines (IL-2, IL-4, IL-6, IL-10, IL-17A, IFN-γ and TNF) were determined using the Ms Th1/Th2/Th17 CBA kit.

Results:
We found that TLR4 deficiency could attenuate the clinical severity and delay the onset of EAN. Moreover, our data showed that the sera levels of IFN-γ, TNF, IL-6 and IL-17A were elevated in the WT mice with EAN when compared with the naive WT mice, but only the production of IL-17A was significantly lower in the TLR4 KO mice with EAN than in their WT counterparts.

Conclusions:
Based on these findings, TLR4 may contribute to the pathogenesis of EAN by regulating Th17 cells and the production of Th17-associated factors. However, the exact mechanism remains unclear and more evidence is needed to elucidate its role in EAN.

eISSN:1896-9151
ISSN:1734-1922