How could CCSVI be related to the immune system, which we know is involved in MS due to genetic studies and effects of immunological treatments?
Billmeik wrote:How could CCSVI be related to the immune system, which we know is involved in MS due to genetic studies and effects of immunological treatments?
so that's why neuros 'know'. Becuase the crabs work so well and because the genetic studies are so conclusive... hmmm
Billmeik wrote:complementary? So you have ccsvi on one hand and an unrelated autoimmune process next to it.
Inflammation in MS is characterized by expression of adhesion molecules,26 followed by a migration of macrophages and T-cells across the BBB. Infiltration of the matrix by macrophages, as in CVD, is considered a crucial step27 (Figure 3A and B). In both situations, macrophages appear with considerable intracellular iron stores due to phagocytosis of senescent erythrocyte. Iron overload in MS plaques has been demonstrated in vivo by MRI.28 In addition, we observed haemosiderin in the urine of patients with active inflammation of MS (personal unpublished data).
Iron-laden macrophages carrying the HFE mutation display increased iron export, increasing the risk of generation of free iron and free radicals, possibly extending tissue lesions.5,6 A study from Australia29 suggests that C282Y-HFE mutation is increased in MS cases of North Western European origin and supports further investigations into the role of iron metabolism in the severity of MS.
As in a venous ulcer, a key determinant of tissue injury is played by MMP9. Exactly as in CVD, the over-expression of MMP9 is insufficiently counterbalanced by its tissue inhibitor TIMP-1. MMP9 can trigger leukocyte transen-dothelial traffic through an altered BBB, and serum active MMP9/TIMP-1 is now considered an appropriate indicator of ongoing MS inflammation.30 Despite histological findings showing haemosiderin deposits encircling the central vein of MS lesions (Figure 2A), the iron-MMP pathway of activation is not considered in MS literature.
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