Experimental autoimmune encephalomyelitis induction in peptidylarginine deiminase 2 knockout mice

2006 ◽  
Vol 498 (2) ◽  
pp. 217-226 ◽  
Author(s):  
Reinout Raijmakers ◽  
Judith Vogelzangs ◽  
Jos Raats ◽  
Maret Panzenbeck ◽  
Maureen Corby ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Knockout Mice ◽  
Peptidylarginine Deiminase ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

Experimental autoimmune encephalomyelitis relapses are reduced in heterozygous golli MBP knockout mice

2003 ◽  
Vol 139 (1-2) ◽  
pp. 44-50 ◽  
Author(s):  
Rhonda R. Voskuhl ◽  
Thomas M. Pribyl ◽  
Kathy Kampf ◽  
Vance Handley ◽  
Hong-biao Liu ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Knockout Mice ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

Beneficial effect of agmatine in the acute phase of experimental autoimmune encephalomyelitis in iNOS-/- knockout mice

2013 ◽  
Vol 206 (2) ◽  
pp. 309-318 ◽  
Author(s):  
Ivana Stevanovic ◽  
Milica Ninkovic ◽  
Ivana Stojanovic ◽  
Srdjan Ljubisavljevic ◽  
Slavica Stojnev ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Beneficial Effect ◽  
Acute Phase ◽  
Knockout Mice ◽  
Autoimmune Encephalomyelitis ◽  
Inos Knockout Mice ◽  
Experimental Autoimmune

p75NTR-knockout mice feature increased axonal vulnerability in experimental autoimmune encephalomyelitis

2007 ◽  
Vol 34 (S 2) ◽  
Author(s):  
S Nessler ◽  
C Stadelmann-Nessler ◽  
A Bittner ◽  
W Jäger ◽  
WH Oertel ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Knockout Mice ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

Aggravated experimental autoimmune encephalomyelitis in IL-15 knockout mice

2010 ◽  
Vol 222 (2) ◽  
pp. 235-242 ◽  
Author(s):  
Diego Gomez-Nicola ◽  
Alessandra Spagnolo ◽  
Carmen Guaza ◽  
Manuel Nieto-Sampedro
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Knockout Mice ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals STEAP4 expression in CNS resident cells promotes Th17 cell-induced autoimmune encephalomyelitis

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Junjie Zhao ◽  
Yun Liao ◽  
William Miller-Little ◽  
Jianxing Xiao ◽  
Caini Liu ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Knockout Mice ◽  
Neutralizing Antibody ◽  
Active Immunization ◽  
Conditional Knockout ◽  
Tissue Destruction ◽  
Autoimmune Encephalomyelitis ◽  
Effector Molecule ◽  
Novel Target ◽  
Experimental Autoimmune

Abstract Background Multiple sclerosis (MS) is a debilitating neurological disease caused by autoimmune destruction of the myelin sheath. Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model for the pathogenesis of MS. We and others have previously demonstrated that IL-17 is critical for the pathogenesis of EAE. The concentration of IL-17 is significantly higher in the sera of MS patients than in healthy controls and correlates with disease activity. Moreover, anti-IL-17 neutralizing antibody demonstrated promising efficacy in a phase II trial in MS patients, further substantiating a key pathogenic role for IL-17 in MS. While Th17 and IL-17 are emerging as a bona fide drivers for neuroinflammation, it remains unclear what effector molecule executes the inflammatory tissue destruction in Th17-driven EAE. Methods By microarray analysis, we found STEAP4 is a downstream molecule of IL-17 signaling in EAE. We then used STEAP4 global knockout mice and STEAP4 conditional knockout mice to test its role in the pathogenesis of EAE. Results Here, we report that the metalloreductase, STEAP4, is a key effector molecule that participates and contributes to the pathogenesis of Th17-mediated neuroinflammation in experimental autoimmune encephalomyelitis. STEAP4 knockout mice displayed delayed onset and reduced severity of EAE induced by active immunization. The reduced disease phenotype was not due to any impact of STEAP4 deficiency on myelin reactive T cells. In contrast, STEAP4 knockout mice were resistant to passively induced EAE, pointing to a role for STEAP4 in the effector stage of EAE. Notably, STEAP4 was only induced the spinal cord of EAE mice that received Th17 cells but not Th1 cells. Consistently, STEAP4 deficiency protected from only Th17 but not Th1-induced EAE. Finally, using Nestin-Cre STEAP4fl/fl mice, we showed that ablation of STEAP4 expression in the resident cells in the central nervous system attenuated disease severity in both active immunization and passive Th17 transfer-induced EAE. Conclusion In this study, we identified STEAP4 as a Th17-specific effector molecule that participates and contributes to the pathogenesis of neuroinflammation, thus potentially provide a novel target for MS therapy.

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