Treatment with Anti-interferon-γ Monoclonal Antibodies Modifies Experimental Autoimmune Encephalomyelitis in Interferon-γ Receptor Knockout Mice

2001 ◽  
Vol 172 (2) ◽  
pp. 460-468 ◽  
Author(s):  
Carmen Espejo ◽  
Milena Penkowa ◽  
Irene Sáez-Torres ◽  
Jordi Xaus ◽  
Antonio Celada ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Knockout Mice ◽  
Interferon Γ ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals Vaccination with DNA Encoding an Immunodominant Myelin Basic Protein Peptide Targeted to Fc of Immunoglobulin G Suppresses Experimental Autoimmune Encephalomyelitis

1998 ◽  
Vol 187 (9) ◽  
pp. 1543-1548 ◽  
Author(s):  
Anna Lobell ◽  
Robert Weissert ◽  
Maria K. Storch ◽  
Cecilia Svanholm ◽  
Katrien L. de Graaf ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
Cell Epitope ◽  
Interferon Γ ◽  
Dna Encoding ◽  
Autoimmune Encephalomyelitis ◽  
The Central Nervous System ◽  
Experimental Autoimmune

We explore here if vaccination with DNA encoding an autoantigenic peptide can suppress autoimmune disease. For this purpose we used experimental autoimmune encephalomyelitis (EAE), which is an autoaggressive disease in the central nervous system and an animal model for multiple sclerosis. Lewis rats were vaccinated with DNA encoding an encephalitogenic T cell epitope, guinea pig myelin basic protein peptide 68–85 (MBP68–85), before induction of EAE with MBP68–85 in complete Freund's adjuvant. Compared to vaccination with a control DNA construct, the vaccination suppressed clinical and histopathological signs of EAE, and reduced the interferon γ production after challenge with MBP68–85. Targeting of the gene product to Fc of IgG was essential for this effect. There were no signs of a Th2 cytokine bias. Our data suggest that DNA vaccines encoding autoantigenic peptides may be useful tools in controlling autoimmune disease.

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

scholarly journals Protective Effect of PBCA Nanoparticles Loaded with Thymulin Against the Relapsing-Remitting Form of Experimental Autoimmune Encephalomyelitis in Mice

2019 ◽  
Vol 20 (21) ◽  
pp. 5374 ◽  
Author(s):  
Sergey M. Lunin ◽  
Maxim O. Khrenov ◽  
Olga V. Glushkova ◽  
Svetlana B. Parfenyuk ◽  
Tatyana V. Novoselova ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
P53 Protein ◽  
Animal Health ◽  
Interferon Γ ◽  
Autoimmune Encephalomyelitis ◽  
Severity Scores ◽  
Cytokine Levels ◽  
Relapsing Remitting ◽  
Jnk Cascade ◽  
Experimental Autoimmune

Relapsing–remitting experimental autoimmune encephalomyelitis (rEAE) in mice is a model that closely resembles relapsing–remitting multiple sclerosis in humans. This study aims to investigate a new approach to modulation of the inflammatory response in rEAE mice using a thymic peptide thymulin bound to polybutylcyanoacrylate (PBCA) nanoparticles. PBCA nanoparticles were used to prolong the presence of thymulin in the blood. Cytokine levels in blood were measured by ELISA; NF-κB and SAPK/JNK cascade activation, as well as Hsp72 and p53 protein expression, were measured by Western blotting. Animal health statuses were estimated using severity scores. Results showed that the cytokine response in rEAE was multi-staged: an early phase was accompanied by an increase in plasma interferon-γ, while the interleukin (IL)-17 response was markedly increased at a later stage. The stages were attributed to rEAE induction and maintenance phases. Thymulin significantly alleviated symptoms of rEAE and lowered plasma cytokine levels both in early and later stages of rEAE, and decreased NF-κB and SAPK/JNK cascade activation. Thymulin modulated NF-kappaB pathway activity via site-specific phosphorylation of RelA/p65 protein (at Ser276 and Ser536). The effect of nanoparticle-bound thymulin was more pronounced than the effect of free thymulin. Therefore, PBCA–thymulin can be considered a prospective treatment for this pathology.

scholarly journals Independent and inter-dependent immunoregulatory effects of NCF1 and NOS2 in experimental autoimmune encephalomyelitis

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Jianghong Zhong ◽  
Anthony C. Y. Yau ◽  
Rikard Holmdahl
Keyword(s):  
Flow Cytometry ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Interferon Γ ◽  
Mouse Strains ◽  
Interleukin 17 ◽  
Autoimmune Encephalomyelitis ◽  
Mediated Effects ◽  
Different Strains ◽  
Deficient Mice ◽  
Experimental Autoimmune

Abstract Background Increasing evidence has suggested that a single nucleotide polymorphism in the Ncf1 gene is associated with experimental autoimmune encephalomyelitis (EAE). However, the mechanisms of NCF1-induced immunoregulatory effects remain poorly understood. In this study, we focus on NCF1 deficiency-mediated effects on EAE in NOS2 dependent and independent ways. Methods To determine the effects of NCF1 and NOS2 during EAE development, we have established recombinant mouse strains deficient at NCF1 and/or NOS2 in a crossbreeding system. Different strains allow us to examine the entire course of the disease in the Nos2-null mice bearing a Ncf1 gene that encodes a mutated NCF1, deficient in triggering oxidative burst, after immunization with recombinant myelin oligodendrocyte glycoprotein (MOG)79-96 peptides. The peptide-induced innate and adaptive immune responses were analyzed by flow cytometry. Results NCF1-deficient mice developed a reduced susceptibility to EAE, whereas NCF1-NOS2 double-deficient mice developed an enhanced EAE, as compared with NOS2-deficient mice. Flow cytometry analyses show that double deficiencies resulted in an increase of neutrophils in the spleen, accompanied with higher release of interleukin-1β in neutrophils prior to EAE onset. The additional deficiency in NCF1 had no added effect on either interleukin-17 or interferon-γ secretion of T cells during the priming phase. Conclusions These studies show that NCF1 and NOS2 interact to regulate peptide-induced EAE.

Interferon-γ Orchestrates the Number and Function of Th17 Cells in Experimental Autoimmune Encephalomyelitis

2011 ◽  
Vol 31 (7) ◽  
pp. 575-587 ◽  
Author(s):  
Nele Berghmans ◽  
Amber Nuyts ◽  
Catherine Uyttenhove ◽  
Jacques Van Snick ◽  
Ghislain Opdenakker ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cells ◽  
Interferon Γ ◽  
Autoimmune Encephalomyelitis ◽  
And Function ◽  
Experimental Autoimmune
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