I don't do video games, but I see the correlation
Post# of 154645
(Total Views: 414)
Posted On: 06/16/2022 9:18:52 PM
I don't do video games, but I see the correlation between the immune system and video games. Strikingly similar.
Every cytokine, every chemokine, every interleukin has a certain purpose. Purposes may change depending on context. Effects, what do they bring? Do they bring weaponry, chemicals necessary for combat? Cellular cascades effecting acid burn and destruction? Maybe they bring strength and vigor, maybe they down regulate.
I wrote this a few weeks back but did not release, it gives an idea as to the effects of some cytokines:
So another reason I was considering for Long Haulers is possibly, the over activity of T-Regulating cells. T-regs suppress or calm down the immune system. But these patients have tons of spike protein and their immune systems should be getting rid of these proteins, and should not be non chalant.
It would be operating in reverse if their T regs cells were over active, or if Interleukin 2 was supplied in excess.
If the T regs were the root of the problem in long haulers, essentially what they would be convinced of is that the spike protein would be "self" and not a foreign antigen.
Somehow, if a macrophage or a dendrite picks up a spike protein and presents it to a T reg, the T reg is supposed to say, that is foreign and allow for and permit the destruction of the spike protein. But rather, if the T reg is at fault, it thinks the spike protein is self and disables the machinery on the presenting cell that would allow for the destruction of the antigen.
Since t regs have developed in the thymus, they know self from nonself and should know the spike is non self and needs to be eliminated, therefore, t regs should not be suppressing the immune system in long haulers.
it is as if the t regs are betraying the covenant they made in the thymus when they were naive t cells being tested whether they can decipher self from non self. The naive t cells which were able to recognize self, were given the choice, either become a t regulator cell or die, because the body doesn't need an auto immune disease.
well, here we have non self, the spike protein, being ignored. really, this is the opposite of an auto immune disease because the body is truly sick, but there is no immune system, b/c the t reg is operating in reverse and suppressing it.
when a t reg wants to suppress a macrophage or a dendrite, an antigen presenting cell, the t reg can take the B7 protein off the macrophage so it can not bind with the CD28 of the t cell (that would engulf it) as a sort of hand shake. by preventing this B7- CD28 handshake b/w the APC and the t-cell, the t cell would then understand that the antigen being presented is actually self and therefore, do not attack the macrophage presenting the antigen. in Long Haulers, it is possible that this handshake is being somehow prevented, but then why would it be again be permitted when LL was introduced? I don't think this is what's happening.
t regs produce a lot of Interleukin 10; the same with macrophages and dendritic cells. Interleukin 10 in excess can take off the MHC 2 major histocompatability complex 2, the tray which the antigen is presented on. IL 10 just takes this off. the APC, so there is no tray and therefore no antigen. essentially, the macrophage has no tray upon which it can present the antigen, thereby disabling it.
but again, when LL is introduced, MHC2 is restored? no, i don't think this is what's happening either.
IL10 reduces Interleukin 12. IL 12 ramps up the acquired arm. But in Long Haulers, the acquired arm of the immune system is dead, so it makes sense that there is increased IL 10 and reduced IL 12. Since there is minimal IL 12, the immune system is dead. That is the case, so there is a lot of IL 10 leading to reduced IL 12.
t regs can not function without Interleukin 2. but IL 2 upregulates immune system when t regs are not around. but when t regs are around, t regs consume all the IL2. none is left for the rest of immune system. IL2 is produced by innate arm. IL 2 amplifies immune system if t regs do not consume it all. t regs have huge number of IL2 receptors. t regs eat up all the IL 2. They remove IL2 from their environment. Since no IL2 is around, the immune response is ramped down and is what was found in long haulers.
Is long haulers the over expression of t reg cells, but by mistake. Somehow, the spike is made to be self? Why the overexpression of IL2? Does the internalization of CCR5 by RANTES somehow induce overexpression of IL2? Does the attachment of LL to CCR5 permit the return of normal level of IL2?
another mechanism is the increased production of TGF beta, tumor growth factor beta, produced by macrophages. This suppresses the immune system. could too much TGF beta be produced in LH, when it should not be? Is TGF beta produced in excess when CCR5 is internalized by CCL5? When LL is added, does the expression of CCR5 on the surface of the cell bring the production of TGF beta back to normal levels?
how does the addition of LL which brings CCR5 back to surface expression play into any of this?
Every cytokine, every chemokine, every interleukin has a certain purpose. Purposes may change depending on context. Effects, what do they bring? Do they bring weaponry, chemicals necessary for combat? Cellular cascades effecting acid burn and destruction? Maybe they bring strength and vigor, maybe they down regulate.
I wrote this a few weeks back but did not release, it gives an idea as to the effects of some cytokines:
So another reason I was considering for Long Haulers is possibly, the over activity of T-Regulating cells. T-regs suppress or calm down the immune system. But these patients have tons of spike protein and their immune systems should be getting rid of these proteins, and should not be non chalant.
It would be operating in reverse if their T regs cells were over active, or if Interleukin 2 was supplied in excess.
If the T regs were the root of the problem in long haulers, essentially what they would be convinced of is that the spike protein would be "self" and not a foreign antigen.
Somehow, if a macrophage or a dendrite picks up a spike protein and presents it to a T reg, the T reg is supposed to say, that is foreign and allow for and permit the destruction of the spike protein. But rather, if the T reg is at fault, it thinks the spike protein is self and disables the machinery on the presenting cell that would allow for the destruction of the antigen.
Since t regs have developed in the thymus, they know self from nonself and should know the spike is non self and needs to be eliminated, therefore, t regs should not be suppressing the immune system in long haulers.
it is as if the t regs are betraying the covenant they made in the thymus when they were naive t cells being tested whether they can decipher self from non self. The naive t cells which were able to recognize self, were given the choice, either become a t regulator cell or die, because the body doesn't need an auto immune disease.
well, here we have non self, the spike protein, being ignored. really, this is the opposite of an auto immune disease because the body is truly sick, but there is no immune system, b/c the t reg is operating in reverse and suppressing it.
when a t reg wants to suppress a macrophage or a dendrite, an antigen presenting cell, the t reg can take the B7 protein off the macrophage so it can not bind with the CD28 of the t cell (that would engulf it) as a sort of hand shake. by preventing this B7- CD28 handshake b/w the APC and the t-cell, the t cell would then understand that the antigen being presented is actually self and therefore, do not attack the macrophage presenting the antigen. in Long Haulers, it is possible that this handshake is being somehow prevented, but then why would it be again be permitted when LL was introduced? I don't think this is what's happening.
t regs produce a lot of Interleukin 10; the same with macrophages and dendritic cells. Interleukin 10 in excess can take off the MHC 2 major histocompatability complex 2, the tray which the antigen is presented on. IL 10 just takes this off. the APC, so there is no tray and therefore no antigen. essentially, the macrophage has no tray upon which it can present the antigen, thereby disabling it.
but again, when LL is introduced, MHC2 is restored? no, i don't think this is what's happening either.
IL10 reduces Interleukin 12. IL 12 ramps up the acquired arm. But in Long Haulers, the acquired arm of the immune system is dead, so it makes sense that there is increased IL 10 and reduced IL 12. Since there is minimal IL 12, the immune system is dead. That is the case, so there is a lot of IL 10 leading to reduced IL 12.
t regs can not function without Interleukin 2. but IL 2 upregulates immune system when t regs are not around. but when t regs are around, t regs consume all the IL2. none is left for the rest of immune system. IL2 is produced by innate arm. IL 2 amplifies immune system if t regs do not consume it all. t regs have huge number of IL2 receptors. t regs eat up all the IL 2. They remove IL2 from their environment. Since no IL2 is around, the immune response is ramped down and is what was found in long haulers.
Is long haulers the over expression of t reg cells, but by mistake. Somehow, the spike is made to be self? Why the overexpression of IL2? Does the internalization of CCR5 by RANTES somehow induce overexpression of IL2? Does the attachment of LL to CCR5 permit the return of normal level of IL2?
another mechanism is the increased production of TGF beta, tumor growth factor beta, produced by macrophages. This suppresses the immune system. could too much TGF beta be produced in LH, when it should not be? Is TGF beta produced in excess when CCR5 is internalized by CCL5? When LL is added, does the expression of CCR5 on the surface of the cell bring the production of TGF beta back to normal levels?
how does the addition of LL which brings CCR5 back to surface expression play into any of this?
(0)
(0)