Abstract
Multiple sclerosis (MS) is a progressive inflammatory and demyelinating disease that affects more than 2.5 million people worldwide every year. Current therapies use mostly disease-modifying drugs, focusing on blocking and regulating systemic functions and the central nervous system (CNS) infiltration of immune cells; however, these therapies only attenuate or delay MS symptoms, but are not effective in halting the disease progression. More recent evidence indicated that regulation of inflammation within the CNS might be a better way to approach the treatment of the disease and microglia, the resident immune cells, may be a promising target of therapeutic studies. Microglia activation classically accompanies MS development, and regulation of microglia function changes the outcome of the disease. In this paper, we review the contributions of microglia to MS pathogenesis and discuss microglial functions in antigen presentation, cytokine release, and phagocytosis. We describe data both from animal and human studies. The significant impact of the timing, intensity, and differentiation fate of activated microglia is discussed, as they can modulate MS outcomes and potentially be critically modified for future therapeutic studies.
Highlights
Multiple sclerosis (MS) is a progressive autoimmune inflammatory and demyelinating disease of the central nervous system (CNS)
MS may be not one disease, but rather a collection of different syndromes presenting themselves with inflammation and demyelination and multiple mechanisms underlying the etiology of the disease
There are other models that induce chemical injury, such as cuprizone, lysolecithin and ethidium bromide, and result in focal demyelination in the white matter. These models are valued for studying the mechanism of demyelination/ remyelination, but they cannot account for the whole picture of MS, because they are devoid of a massive leukocyte infiltration [13, 15, 16]
Summary
Multiple sclerosis (MS) is a progressive autoimmune inflammatory and demyelinating disease of the central nervous system (CNS). These models are valued for studying the mechanism of demyelination/ remyelination (as remyelination is initiated upon termination of the chemical injury reagent), but they cannot account for the whole picture of MS, because they are devoid of a massive leukocyte infiltration [13, 15, 16] Compared to these models, EAE, even though it has the drawback that the disease onset is due to a defined antigen presentation as opposed to MS, appears to relatively better reflect and recapitulate critical features and progressions of MS; most of the current mechanism studies and treatments for MS still mainly rely on EAE models [17]. We discuss functions of microglia in MS, EAE and other experimental studies and review evidence implicating the critical roles of microglia in the complicated neural-immune networks
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