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Meningeal inflammation plays a role in the pathology of primary progressive multiple sclerosis
These cytokines not only accelerate degradation of the cartilage matrix but also amplify the local inflammatory response via autocrine or paracrine signaling (13)
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This pathology results from persistently thwarted attempts at normal DNA replication, DNA repair, and cell division, and produces abnormally large red cells called megaloblasts (and hypersegmented neutrophils) with abundant cytoplasm capable of RNA and protein synthesis, but with clumping and fragmentation of nuclear chromatin
It inhibits NF-B pathway activation, reducing the production of pro-inflammatory cytokines such as IL-1, IL-6, and TNF- [130, 131]
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