Arneth B. Contributions of T cells in multiple sclerosis: what do we currently know? J Neurol. 2020 Oct 20. doi: 10.1007/s00415-020-10275-x. Epub ahead of print.
Background: Multiple sclerosis (MS) is a complex autoimmune disorder characterized by neurologic dysfunction. The symptoms worsen as the disease progresses to the relapsing stage.
Aim: This study aimed to examine the role of T cells in MS pathogenesis.
Materials and methods: The review was performed based on articles obtained from PsycINFO, PubMed, Web of Science, and CINAHL. Search terms and phrases, such as “multiple sclerosis,” “MS,” “T cells,” “development,” “Dysregulated T cells,” and “Effector T cells”, were used to identify articles that could help explore the research topic.
Results: The pathogenesis of MS is linked to the regulatory, inflammatory, suppressive, and effector roles of T cells. However, the actual roles of specific T cell subsets in MS development are not well understood (Why not?).
Discussion: The study revealed a significant link between MS and T cell activity. Targeting T cells is a potential strategy for the development of new therapies to manage MS.
Conclusion: MS is a complex demyelinating condition that affects several million people around the world. Research has revealed that various classes of T cells, including effector T cells and regulatory T cells, influence the development and progression of MS. Further investigations are required to elucidate the underlying mechanisms through which specific T cell populations influence MS pathogenesis.
I guess these type of posts are like abit of bait for me and I feel compelled to respond……..So to keep an open mind I will say this. I search “multiple sclerosis”, “ice berg” “frozen water” “icicle” and discover that there could be a link between the “Titanic” and multiple sclerosis…OK I am talking BS but you find what you are looking for…….It’s behind you
MS is caused by a Kitty. Which one do you kill? The cute little white ones? The black one? Or the ruddy big one that’s behind you that is about to club you to death? It depends where you are looking at the time
Why is it important….because it determines where you go next?
The logical position is that it is abit of both B and T cell activity, but in some peoples eyes, this is OK as long as the T cells are the most important targets. Response to therapy in MS however may put the B cells in accendency. The yin and yang of immune ideas is also occuring in remyelination.
Which of the remyelination schools is correct?
(a) Myelinating cells come from immature cells as typically seen in animals (Franklin School) or from (b) surviving oligodendrocytes as suggested in humans (Frisen school). The humans guys held out an olive branch and said although the majority of people with MS exhibited little evidence of new oligodendrocyte generation, about a quarter showed a more than threefold increase in the generation of new oligodendrocytes in normal appearing white matter, demonstrating the potential to greatly increase oligodendrocyte generation in the adult human MS brain, like that which occurs in animals. It is suggested that this may create myelin in in a way that is indisguishiable from that which was present before demyelination and it may not be a shadow plaque that the pathologiists had said was remyelination. Therefore perhaps saying the pathologists are abit rubbish becuase they didn’t spot this issue. So the remyelinationers unite. Sad to say the pathologists seem to have run a mile to keep out of the argument (OK I am being abit provocative here).
Therefore, what has emerged are (at least) two distinct mechanisms of new myelin formation following demyelination – one involving the generation of new oligodendrocytes, and one with new myelin formed by existing oligodendrocyte
There may be differences between how grey and white matter reemylinate and age may come into play that creates focuses of difference between rodents of humans, but the consensus is that human cells can fundementally repair like rodent cells, but remylination by progenitors is more efficient than by mature cells.
So again why is it important where the emphasis is placed. It iis importnat because it is where to put emphasis on treatements. I suspect like the T and B debate the progenitor verse oligodendrocyte repair debate will be biased in one direction will it be the right one?
Revisiting remyelination: Towards a consensus on the regeneration of CNS myelin.Franklin RJM, Frisén J, Lyons DA.Semin Cell Dev Biol. 2020 Oct 17:S1084-9521(20)30157-9.The biology of CNS remyelination has attracted considerable interest in recent years because of its translational potential to yield regenerative therapies for the treatment of chronic and progressive demyelinating diseases such as multiple sclerosis (MS). Critical to devising myelin regenerative therapies is a detailed understanding of how remyelination occurs. The accepted dogma, based on animal studies, has been that the myelin sheaths of remyelination are made by oligodendrocytes newly generated from adult oligodendrocyte progenitor cells in a classical regenerative process of progenitor migration, proliferation and differentiation. However, recent human and a growing number of animal studies have revealed a second mode of remyelination in which mature oligodendrocytes surviving within an area of demyelination are able to regenerate new myelin sheaths. This discovery, while opening up new opportunities for therapeutic remyelination, has also raised the question of whether there are fundamental differences in myelin regeneration between humans and some of the species in which experimental remyelination studies are conducted. Here we review how this second mode of remyelination can be integrated into a wider and revised framework for understanding remyelination in which apparent species differences can be reconciled but that also raises important questions for future research.