Experimental Autoimmune Encephalomyelitis in the Mouse

Sd, Miller; Wj, Karpus; Miller, Stephen D.

doi:10.1002/0471142735.im1501s88

Cited by 193 publications

(222 citation statements)

References 66 publications

Supporting

Mentioning

216

Contrasting

Unclassified

Order By: Relevance

“…In EAE, the antigens responsible for the disease have been described. By immunizing the animal with myelin proteins such as MBP, proteolipid protein or myelin oligodendrocyte glycoprotein (MOG), disease can be induced [78] . In humans, such common antigens remain unknown in spite of several attempts to identify them [25,30] .…”

Section: Role Of B Cellsmentioning

confidence: 99%

Multiple sclerosis and the role of immune cells

Høglund

Maghazachi

2014

WJEM

131

101

View full text Add to dashboard Cite

Multiple sclerosis (MS) is a complex disease with many different immune cells involved in its pathogenesis, and in particular T cells as the most recognized cell type. Recently, the innate immune system has also been researched for its effect on the disease. Hence, cells of the immune system play vital roles in either ameliorating or exacerbating the disease. The genetic and environmental factors, as well as the etiology and pathogenesis are of utmost importance for the development of MS. An insight into the roles play by T cells, B cells, natural killer cells, and dendritic cells in MS and the animal model experimental autoimmune encephalomyelitis, will be presented. Understanding the mechanisms of action for current therapeutic modalities should help developing new therapeutic tools to treat this disease and other autoimmune diseases.

show abstract

Section: Role Of B Cellsmentioning

confidence: 99%

Multiple sclerosis and the role of immune cells

Høglund

Maghazachi

2014

WJEM

131

101

View full text Add to dashboard Cite

show abstract

“…The effector phase consists of migration of activated myelin-specific T cells to the CNS, elaboration of chemokines and cytokines (e.g. IFN-g, TNF-a and IL-17), activation of peripheral monocytes/macrophages and CNS-resident microglial cells (Miller et al, 2007;Stephen et al, 2007). Since, in MOG peptide-induced EAE both spinal cord and forebrain regions were attacked simultaneously (Girolamo et al, 2011;Kuerten et al, 2007;Merkler et al, 2006), in this experiment we evaluate cerebral cortex region in C57BL/6 mice by focusing on inflammatory responses, BBB dysfunction and trans-endothelium migration of immune cells.…”

Section: Discussionmentioning

confidence: 99%

Prophylactic Effect of BIO-1211 Small-Molecule Antagonist of VLA-4 in the EAE Mouse Model of Multiple Sclerosis

Ramroodi

Khani

Ganjali

et al. 2015

Immunological Investigations

View full text Add to dashboard Cite

show abstract

“…EAE induction. EAE was induced basically as described previously (23). Briefly, mice were subjected to subcutaneous injection of myelin/ oligodendrocyte glycoprotein (MOG; 150 g) peptide (amino acids 35 to 55)-0.1 ml of complete Freund's adjuvant (CFA) emulsion containing 400 g of Mycobacterium tuberculosis (Difco) on day 0.…”

Section: Methodsmentioning

confidence: 99%

“…Subsequently, the mice received intraperitoneal injection of 200 ng of pertussis toxin (List Biological Laboratories) on days 0 and 2. Disease states of EAE were assessed and given the following scores: 0, no sign of disease; 1, limp tail or hind limb weakness; 2, partial hind limb paralysis; 3, complete hind limb paralysis (23).…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, we next evaluated inflammatory status in experimental autoimmune encephalomyelitis (EAE), a murine model of neuronal autoimmune disease which is well known to closely mimic the inflammatory demyelinating diseases, including multiple sclerosis (12). WIM-6 mice were immunized with myelin oligodendrocyte glycoprotein (MOG; amino acids 35 to 55) and monitored daily to assign neurological severity scores of the EAE symptoms (EAE score [23]). By 10 days after the immunization (day 10), 69% of the ICR strain mice exhibited neurological disorders characterized by hypotonus of the tail muscle (Fig.…”

Section: Generation Of the Hil6-bac-luc Transgenic (Wim-6) Micementioning

confidence: 99%

See 1 more Smart Citation

Whole-Body In Vivo Monitoring of Inflammatory Diseases Exploiting Human Interleukin 6-Luciferase Transgenic Mice

Hayashi

Takai

et al. 2015

Molecular and Cellular Biology

View full text Add to dashboard Cite

Chronic inflammation underlies the pathological progression of various diseases, and thus many efforts have been made to quantitatively evaluate the inflammatory status of the diseases. In this study, we generated a highly sensitive inflammation-monitoring mouse system using a bacterial artificial chromosome (BAC) clone containing extended flanking sequences of the human interleukin 6 gene (hIL6) locus, in which the luciferase (Luc) reporter gene is integrated (hIL6-BAC-Luc). We successfully monitored lipopolysaccharide-induced systemic inflammation in various tissues of the hIL6-BAC-Luc mice using an in vivo bioluminescence imaging system. When two chronic inflammatory disease models, i.e., a genetic model of atopic dermatitis and a model of experimental autoimmune encephalomyelitis (EAE), were applied to the hIL6-BAC-Luc mice, luciferase bioluminescence was specifically detected in the atopic skin lesion and central nervous system, respectively. Moreover, the Luc activities correlated well with the disease severity. Nrf2 is a master transcription factor that regulates antioxidative and detoxification enzyme genes. Upon EAE induction, the Nrf2-deficient mice crossed with the hIL6-BAC-Luc mice exhibited enhanced neurological symptoms concomitantly with robust luciferase luminescence in the neuronal tissue. Thus, whole-body in vivo monitoring using the hIL6-BAC-Luc transgenic system (WIM-6 system) provides a new and powerful diagnostic tool for real-time in vivo monitoring of inflammatory status in multiple different disease models. E xposure to environmental xenobiotics and the accompanying production of cellular oxidative stress give rise to a wide variety of inflammatory diseases in modern society (reviewed in references 1 and 2). To take a step against the widespread prevalence of inflammation-related diseases or low-grade systemic inflammations, it is crucial to elucidate the mechanistic basis for the cellular response to the inflammation. In this aspect, development of an in vivo monitoring system for evaluation of inflammatory status and validation of therapeutic agents has been eagerly awaited. Accurate and sensitive inflammation-monitoring animal models will accelerate further study of inflammatory diseases and development of new therapeutics.Inflammatory stimuli induce gene expression of a series of proinflammatory cytokines, such as tumor necrosis factor (TNF), interleukin 1␤ (IL-1␤), and IL-6. Among the proinflammatory cytokines, IL-6 is a key cytokine that is produced by many types of cells, including immune cells (e.g., macrophages and T and B lymphocytes), hepatocytes, glial cells, and fibroblasts (reviewed in reference 3). Expression of IL-6 in resting immune cells is usually suppressed, while it is rapidly induced upon exposure to a variety of inflammatory stimuli (reviewed in reference 4). Subsequently, the induced IL-6 participates in multiple physiological and pathological processes, including innate and acquired immune responses and pathogenesis of autoimmune inflammatory diseases. This sensi...

show abstract

Experimental Autoimmune Encephalomyelitis in the Mouse

Cited by 193 publications

References 66 publications

Multiple sclerosis and the role of immune cells

Multiple sclerosis and the role of immune cells

Prophylactic Effect of BIO-1211 Small-Molecule Antagonist of VLA-4 in the EAE Mouse Model of Multiple Sclerosis

Whole-Body In Vivo Monitoring of Inflammatory Diseases Exploiting Human Interleukin 6-Luciferase Transgenic Mice

Contact Info

Product

Resources

About