relating to immune system

[kim]

I have found this to be an interesting site with lots of idea's that seem useful relating to PANDAS. These are excerpts from a few. The first article has something specific to a PM message, but thought I would share it here anyway. bolding mine

 

 

The multiple sclerosis resource center

 

http://www.msrc.co.uk/index.cfm?fuseaction...FTOKEN=89832361

 

The U-M research team conducted the studies in mice that have a disease similar to MS: experimental autoimmune encephalomyelitis or EAE. The team found that different inflammatory chemicals, whose activity is linked to two different types of immune system T cells, could bring on the same paralysis and other MS-like signs. They also showed that drugs that block one of the inflammation pathways were not effective at blocking the other. The results, published online ahead of print, will appear in the July 7 issue of the Journal of Experimental Medicine.

 

 

http://www.msrc.co.uk/index.cfm?fuseaction...FTOKEN=89832361

 

Clonal expansion of B cells and the production of oligoclonal IgG in the brain and cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS) have long been interpreted as circumstantial evidence of the immune-mediated pathogenesis of the disease and suggest a possible infectious cause.

 

Extensive work on intrathecally produced antibodies has not yet clarified whether they are pathogenetically relevant. Irrespective of antibody specificity, however, the processes of antibody synthesis in the CNS of patients with MS are becoming increasingly clear. Likewise, targeting B cells might be therapeutically relevant in MS and other autoimmune diseases that are deemed to be driven predominantly by T cells.

 

Accumulating evidence indicates that in MS, similar to rheumatoid arthritis, B cells aggregate into lymphoid-like structures in the target organ. The process of aggregation is mediated through the expression of lymphoid-homing chemokines.

 

In the brain of a patient with MS, ectopic B-cell follicles preferentially adjoin the pial membrane within the subarachnoid space. Recent findings indicate that substantial numbers of B cells that are infected with Epstein-Barr virus (EBV) accumulate in these intrameningeal follicles and in white matter lesions and are probably the target of a cytotoxic immune response.

 

These findings, which await confirmation, could be an explanation for the continuous B-cell and T-cell activation in MS, but leave open concerns about the possible pathogenicity of autoantibodies.

 

Going beyond the antimyelin-antibody dogma, the above data warrant further work on various B-cell-related mechanisms, including investigation of B-cell effector and regulatory functions, definition of the consistency of CNS colonisation by Epstein-Barr virus-infected B cells, and understanding of the mechanisms that underlie the formation and persistence of tertiary lymphoid tissues in patients with MS and other chronic autoimmune diseases (ectopic follicle syndromes). This work will stimulate new and unconventional ways of reasoning about MS pathogenesis.

 

Source: Lancet Neurology 2008; 7:852-858 © 2008 Elsevier Limited (12/08/08)

 

 

http://www.msrc.co.uk/index.cfm?fuseaction...FTOKEN=89832361

 

 

Researchers prove the role of certain leukocyte cell adhesion molecules in the pathogenesis of the disease.

 

 

The results clearly demonstrate that CD166/ALCAM is involved in the inflammatory process by priming the migration of leukocytes across the blood-brain barrier (BBB). The research project combines results using an in vitro human BBB model and an in vivo experimental autoimmune encephalomyelitis mouse model. Normally, a limited number of immune cells are able to cross the BBB and penetrate the central nervous system. In MS and other neuroinflammatory diseases, the increased permeability of the BBB is associated with an increase in the transmigration of some of these immune cells, which penetrate the central nervous system and cause the demyelinating lesions of MS. A previous study by Dr. Prat's team published in October in Nature Medicine (1), proved that a certain type of leukocyte, the TH17 lymphocyte, produces two critical products, interleukins 17 and 22 (IL-17 and IL-22), which contribute to infiltrating the blood-brain barrier and causing inflammation of the central nervous system.

 

"Blocking the migration of immune cells across the BBB has long been considered a promising therapeutic approach to autoimmune diseases of the central nervous system," states Dr. Prat. "This study has given us new insight into the factors involved in the pathogenesis of immune reactions affecting the central nervous system and allowed us to identify potential targets to suppress neuroinflammatory processes.