Multipe Sclerosis - Pathology

Autoimmune inflammatory disease - updated: 26 October 2009

Multiple sclerosis, an autoimmune inflammatory disease: prospects for its integrative management

Altern Med Rev. 2001 Dec;6(6):540-66

Kidd PM.

often debilitating disease, MS features autoimmune inflammatory attack against the myelin insulation of neurons. Thymus derived (T) cells sensitized against myelin self-antigens secrete tumor necrosis factor, cytokines, prostaglandins, and other inflammatory mediators that strip away the myelin and sometimes destroy the axons. Familial and twin inheritance studies indicate MS is mildly heritable. No single MS locus has been identified, but an HLA haplotype has been implicated. Unique geographic distribution of the disease is best attributed to some combination of vitamin D abnormality and dietary patterns. No pharmaceutical or other therapies exist that confer prolonged remission on MS, and obvious interrelationships between toxic, infectious, and dietary factors make a persuasive case for integrative management. The time-proven MS diet meticulously keeps saturated fats low, includes three fish meals per week, and eliminates allergenic foods. Dietary supplementation for MS minimally requires potent vitamin supplementation, along with the thiol antioxidants, the anti-inflammatory omega-3 fatty acids, and adaptogenic phytonutrients. Gut malabsorption and dysbiosis can be corrected using digestive enzymes and probiotics. Long-term hyperbaric oxygen therapy can slow or remit the disease. Transdermal histamine offers promise, and adenosine monophosphate may sometimes benefit. Chronic viruses and other infectious load must be aggressively treated and exercise should maintain muscle tone and balance. Early intervention with integrative modalities has the potential to make MS a truly manageable disease.

Publication Types:

• Review

Autoantibodies in inflammatory demyelinating diseases of the central nervous system

Swiss Med Wkly. 2008 Nov 29;138(47-48):692-707

Lalive PH.

The determination of disease-specific autoantibodies (Abs) is a challenge in any autoimmune disease. The significance of Abs detected in inflammatory demyelinating diseases (IDD) of the central nervous system (CNS), such as multiple sclerosis (MS), is still unclear. Histopathological reports have demonstrated that a humoral (Abs)-mediated pattern of demyelination is detected in >50% of MS patients and is consistently associated with active demyelination. The observation that these patients specifically respond to plasmapheresis reinforces the hypothesis of a specific humoral MS subtype. One of the most intensively studied antigen targets in MS is a glycoprotein of the myelin sheath called the Myelin Oligodendrocyte Glycoprotein (MOG). Recent advances have shown that epitope specificity of MOG is crucial in terms of specificity of the Ab response. Several other auto-Abs, including anti-myelin, oligodendrocyte and neuronal Abs have been studied in MS. These auto-Abs may have pathogenic or protective properties, but could also have no functional role. Recently, the demonstration of a highly specific auto-Ab in an IDD of the CNS called neuromyelitis optica (NMO), directed against the aquaporin-4 (AQP-4) located at the blood brain barrier (BBB), has allowed a refinement of the diagnostic criteria of NMO and classification of this disease as an autoimmune channelopathy. These recent advances have reinforced the interest in tracking the role of the humoral response in the different IDD of the CNS.

Publication Types:

• Review

CD4 T cells: Balancing the coming and going of autoimmune-mediated inflammation in the CNS

: Brain Behav Immun. 2008 May;22(4):421-30

Dittel BN.

The regulation of the inflammatory response is often viewed as very complex with many cellular players. The type of immune response generated is dependent upon the nature of the immune stimulation. In autoimmunity, one of the most important players is the CD4 T cell. The CD4 T cell lineage consists of a number of phenotypically and functionally distinct subsets. The unique functions of CD4 T cells are often mediated by soluble factors, which shape the nature of the immune response. In a T cell-mediated autoimmune response, such as in multiple sclerosis (MS), the CD4 T cell is thought to orchestrate and drive the immune response resulting in inflammation within the central nervous system (CNS). The extent of the inflammation must be tightly controlled or permanent tissue damage will occur. In MS, progressive debilitating disease is thought to be due to such damage. In addition to promoting inflammation, the CD4 T cell lineage also has the capacity to prevent and downmodulate inflammation. This is accomplished by specific CD4 T regulatory (Treg) cells and other regulatory feedback mechanisms. Thus although the complexity of the immune system is often viewed as too complicated for a nonimmunologist to fully understand, there are patterns that emerge that make the system clearer. One such pattern is the balance that the immune system must always maintain. A weak or slow immune response to a pathogen can lead to sickness and even death, while a too robust or uncontrolled immune response can lead to tissue damage, and for autoimmune diseases, ultimately death. How CD4 T cells maintain this balance will be discussed in the context of the CNS autoimmune disease MS.

Publication Types:

• Review

Publication Types:

• Review