E xperimental autoimmune encephalomyelitis (EAE) has served as a prototypic model of T cell–mediated, organspecific autoimmune disease, and as a useful model for the human disease, multiple sclerosis (MS) (1). Frei et al. (2) demonstrate that in two strains of mice with a double knockout, where both TNFand LTare inactivated, that EAE may develop. The disease in these double knockout mice progre...

Multiple sclerosis (MS) is believed to be initiated by myelin-reactive CD4(+) Th cells. IL-12-polarized Th1 cells, IL-23-polarized Th17 cells, and Th17 cells that acquire Th1 characteristics were each implicated in autoimmune pathogenesis. It is debated whether Th cells that can drive the development of demyelinating lesions are phenotypically diverse or arise from a single lineage. In the curr...

BACKGROUND: Immunity against the T cell receptor (TCR) is considered to play a central role in the regulation of experimental allergic encephalomyelitis (EAE), a model system of autoimmune disease characterized by a restricted usage of TCR genes. Methods of specific vaccination against the TCR of pathogenetic T cells have included attenuated T cells and synthetic peptides from the sequence of t...

In mice affected with equine encephalomyelitis, the first pathological disturbance in infant animals is an inflammatory reaction, which is usually less pronounced in adult animals. A characteristic type of parenchymal damage appears to be independent of the inflammation. In such foci of injury there is initially a vacuolation of intercellular tissue. Neurones in such areas are at first intact, ...

T cells reacting to self-components can promote tissue damage when escaping tolerogenic control mechanisms which may result in autoimmune disease. The current treatments for these disorders are not antigen (Ag) specific and can compromise host immunity through chronic suppression. We have previously demonstrated that co-administration of encapsulated or free Ag with tolerogenic nanoparticles (t...

Regulation of inflammation in the CNS is essential to prevent irreversible cellular damage that can occur in neurodegenerative diseases such as multiple sclerosis (MS). We investigated the role of interleukin-4 (IL-4) in regulating CNS inflammation using the animal model of MS, experimental autoimmune encephalomyelitis (EAE). We found that CNS-derived IL-4 was a critical regulator because mice ...

Extensive research has been devoted to the study of IFNfunction in several autoimmune diseases. Previously considered the hallmark of Th1 differentiation and pro-inflammatory responses, it has soon become evident that this pivotal cytokine plays a much more complex role than initially thought. These considerations have been particularly relevant to the understanding of the pathogenesis of autoi...

A negative correlation between the geographical distribution of autoimmune diseases and helminth infections has been largely associated in the last few years with a possible role for such type of parasites in the regulation of inflammatory diseases, suggesting new pathways for drug development. However, few helminth-derived immunomodulators have been tested in experimental autoimmune encephalom...

Multiple sclerosis (MS) is the principal cause of autoimmune neuroinflammation in humans, and its animal model, experimental autoimmune encephalomyelitis (EAE), is widely used to gain insight about their immunopathological mechanisms for and the development of novel therapies for MS. Most studies on the role of interferon (IFN)-γ in the pathogenesis and progression of EAE have focused on periph...