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The immune system has an inherent contradiction in the way it functions – the major role of the immune system is to fight off the invasion of our bodies by bacteria, fungi, viruses and parasites; but in order to accomplish this, immune cells need to recognize our own tissues so that they can determine what is foreign when we have an infection.

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2018 May 30. doi: 10.1089/rej.2017.2049

Abstract

Proteostasis, which includes the repair and disposal of misfolded proteins, depends, in part, on the activity of heat shock proteins (HSPs), a well-known class of chaperone molecules. When this process fails, abnormally folded proteins may accumulate in cells, tissues, and blood. These species are a hallmark of protein aggregation diseases, but also amass during aging, often in the absence of an identified clinical disorder.

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We have worked on the JC virus for many months to understand how this virus travels to the brain causing PML (Progressive Multifocal Leukoencephalopathy) a serious and potentially fatal infection which complicates a number of MS therapies including Tysabri, Tecfidera, Gilenya, Ocrevus and Lemtrada. This infection also complicates treatments for other autoimmune diseases, transplantation and chemotherapy; and is seen in different immune deficiencies and HIV-AIDS. There are at least 15 monoclonal antibody treatments for different conditions which are complicated by the JC virus.

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Most data supports that the major culprit in the formation of Multiple Sclerosis is the T-cell, which is a white blood cell that plays a key role in the immune system. These cells are named after the small organ – the thymus gland – where they are produced. In particular, MS is an immune-mediated autoimmune disease caused, in all probability, by a defect in regulatory T-cells: cells which regulate, or maintain order in the immune system, and suppress immune responses either by cell-cell contact or by secreting cytokines (proteins) to regulate the extent of potentially damaging inflammation to the tissues of the body. Unrestrained activation of effector T cells (normally controlled by regulatory T cells) allows them to produce pro-inflammatory cytokines and recruit other inflammatory immune cells to a tissue causing damage such as myelin injury as seen in MS. The consequence of inflammation in MS, in all probability, is a chronic neurodegenerative process called Progressive MS, which is an additional level of complexity that is being intensively investigated.

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FIND, STOP, CURE MS