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T Cell Apoptosis In Multiple Sclerosis And Experimental Autoimmune Encephalomyelitis
Funder
National Health and Medical Research Council
Funding Amount
$299,950.00
Summary
Multiple sclerosis is a disease of the nervous system and is a common cause of disability in young adults. There is increasing evidence that multiple sclerosis is caused by repeated attacks on the nervous system by the white blood cells (lymphocytes) of the body's own immune system. A major unanswered question in multiple sclerosis is why repeated immune attacks on the nervous system occur. I have recently proposed that the repeated nature of the immune attacks in multiple sclerosis results from ....Multiple sclerosis is a disease of the nervous system and is a common cause of disability in young adults. There is increasing evidence that multiple sclerosis is caused by repeated attacks on the nervous system by the white blood cells (lymphocytes) of the body's own immune system. A major unanswered question in multiple sclerosis is why repeated immune attacks on the nervous system occur. I have recently proposed that the repeated nature of the immune attacks in multiple sclerosis results from a failure of the mechanism that switches off immune attacks on the nervous system in healthy individuals. In an animal model of multiple sclerosis we have shown that the lymphocytes attacking the nervous system rapidly commit suicide in the nervous system by a process known as apoptosis, and that this is associated with switching off of the immune attack and recovery from the disease. The present project aims to study further this process of lymphocyte suicide in experimental animals by determining whether the lymphocyte suicide is mediated through a death receptor molecule named Fas (CD95). The project will also investigate the process of lymphocyte suicide in white blood cells obtained from patients with multiple sclerosis to determine if this process is defective and to determine whether these patients have abnormalities in the Fas molecular pathway. This project will shed light on the question of why repeated immune attacks on the nervous system occur in multiple sclerosis, and has the potential to lead to the development of new treatments for multiple sclerosis.Read moreRead less
Pathogenesis Of Inflammatory Demyelinating Polyneuropathy
Funder
National Health and Medical Research Council
Funding Amount
$421,980.00
Summary
This project will investigate the cause of Guillain Barre syndrome (GBS), a severe disease that causes paralysis of the limbs, and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), a similar disease that causes either repeated attacks of weakness or chronic weakness. These are important diseases of the peripheral nervous system. In GBS and CIDP, white blood cells move from the bloodstream to phagacytose (eat) the myelin that surrounds peripheral nerve fibres. Removal of myelin interferes ....This project will investigate the cause of Guillain Barre syndrome (GBS), a severe disease that causes paralysis of the limbs, and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), a similar disease that causes either repeated attacks of weakness or chronic weakness. These are important diseases of the peripheral nervous system. In GBS and CIDP, white blood cells move from the bloodstream to phagacytose (eat) the myelin that surrounds peripheral nerve fibres. Removal of myelin interferes with normal function of the nerves. The project will investigate 5 aspects of GBS and CIDP. (1) We will determine which component of myelin is recognised by white blood cells from patients with GBS and CIDP. We have performed preliminary studies indicating that a protein known as PMP-22 and gangliosides may be targets of the immune attack, but this needs to be confirmed. (2) We will study how the immune attack is turned off in GBS. (3) We will study whether and why the immune attack fails to be turned off in CIDP. (4) We will identify genetic markers that may predispose to GBS and CIDP. (5) We will investigate a novel animal model of GBS that we have induced in rats by inoculation with fragments of PMP-22 protein.Read moreRead less