To boost or supress autoimmunity, that is the question

[MSUK]

Breaking peripheral immune tolerance to CNS antigens in neurodegenerative diseases: Boosting autoimmunity to fight-off chronic neuroinflammation.

Schwartz M, Baruch K.

Abstract

Immune cell infiltration to the brain's territory was considered for decades to reflect a pathological process in which immune cells attack the central nervous system (CNS); such a process is observed in the inflammatory autoimmune disease, multiple sclerosis (MS).

As neuroinflammatory processes within the CNS parenchyma are also common to other CNS pathologies, regardless of their etiology, including neurodegenerative disorders such as Alzheimer's disease (AD) and Amyotrophic lateral sclerosis (ALS), these pathologies have often been compared to MS, a disease that benefits from immunosuppressive therapy.

Yet, over the last decade, it became clear that autoimmunity has a bright side, and that it plays a pivotal role in CNS repair following damage. Specifically, autoimmune T cells were found to facilitate CNS healing processes, such as in the case of sterile mechanical injuries to the brain or the spinal cord, mental stress, or biochemical insults. Even more intriguingly, autoimmune T cells were found to be involved in supporting fundamental processes of brain functional integrity, such as in the maintenance of life-long brain plasticity, including spatial learning and memory, and neurogenesis.

Importantly, autoimmune T cells are part of a cellular network which, to operate efficiently and safely, requires tight regulation by other immune cell populations, such as regulatory T cells, which are indispensable for maintenance of immunological self-tolerance and homeostasis.
Here, we suggest that dysregulation of the balance between peripheral immune suppression, on one hand, and protective autoimmunity, on the other, is an underlying mechanism in the emergence and progression of the neuroinflammatory response associated with chronic neurodegenerative diseases and brain aging.

Mitigating chronic neuroinflammation under these conditions necessitates activation, rather than suppression, of the peripheral immune response directed against self.

Accordingly, we propose that fighting off acute and chronic neurodegenerative conditions requires breaking peripheral immune tolerance to CNS self-antigens, in order to boost protective autoimmunity. Nevertheless, the optimal approach to fine tune such immune response must be individually explored for each condition.

Source: J Autoimmun. 2014 Sep 5. pii: S0896-8411(14)00127-9. doi: 10.1016/j.jaut.2014.08.002 © 2014 Elsevier Ltd & Pubmed PMID: 25199710 (11/09/14) http://www.ms-uk.org/immunecells

[pawel96]

Hm, so maybe in the end there is something in Marshall Protocol? Regarding boosting the immune system rather then suppresing it?

P.

[SeanReynolds]

If you look at the MAP or CPn thesis of MS causation, clearly boosting the immune system actually just helps you fight the supposed causative bacterial infection better. eg Vit D, multivits, interferon which is an immune booster albeit with nasty side effects, or indeed antibiotics. So it's a rather obvious outcome.

[frodo]

It can be misleading to simplify so much the question. The immune system is not just one thing, but a system composed by hundred of different components. It is clear that in MS it does not work properly, and therefore some parts will have to be boosted and others suppressed to compensate the wrong behaviour.

According to the recent investigations, EBV-infected B-cells are not the main culprit. Nearly everybody has them but only a few develop MS. Now the focus is in CD8+ T-cells, that in normal person would attack and destroy those infected B-cells and for some reason they fail in MS (Defective T-cell control of Epstein–Barr virus infection in multiple sclerosis, http://www.nature.com/cti/journal/v6/n1 ... 1687a.html). Interestingly, they are the same cells that appear in the lesions.

Therefore the solution will be a mixture. In the future B-cells will be depleted with anti-CD20 or something similar and at the same time CD8+ cells will have to be boosted.

[SeanReynolds]

If you look at the CPn (or even MAP) thesis, it is a very simple explanation indeed.

Dr Wheldon points to EBV, HHV-6 and potentially other viral diseases as facilitating more and more ingress by the CPn bacterium. This fits all the data raised so far perfectly.

http://www.davidwheldon.co.uk/hhv6.html

I find the auto-immune line of enquiry to be the biggest red herring and false trail of the past 50 years.