Of Tolerance and TRUTH

          Have you ever heard the saying, “What you don’t know can’t hurt you”, or, “Ignorance is bliss”? Well I’m here to tell you it’s a lie. [Lyme Disease], or more correctly Relapsing Fever Borrelliosis/Post-Sepsis Syndrome does hurt in more ways than one. It’s real! The physical, mental and financial toll it takes. The lives of millions that are destroyed. Most likely what you do know from either your own experience or from what you have been told is only the tip of the iceberg.

Oh, and there’s so very much more underneath. Deliberately being hid from you so that the crooks who changed the case definition could profit off of testing and vaccines at your expense. Yup, lies upon lies, upon lies.

Iceberg-Feature-Meme

Did you know that spirochetes attack and permanently destroy your immune system? Did you know that their outer surface proteins (Osps), are shed and are variable, so as to evade your immune system? It’s to keep your body from making antibodies. The 2-tiered test was designed to only detect 15% of those who have a HLA-linked gene, not the 85% of us with debilitating neurologic symptoms and immunosuppression.

How many really understand what this damage does, and how it is basically permanent and the allusion to a cure from such as ILADS is false? To fully understand how your immune system is damaged you must look below the surface of lies and the fraud of the perpetrators of the LYME CRYME against humanity. Of misinformed, (however well-meaning ), friends, doctors, and yes, Facebook “Experts”.

You have to follow the science, connect the dots and think critically for yourself. Your life as well as countless others depends on it.

A Osp is an outer surface protein on a spirochete.  They are labeled alphabetically, coincidentally the first one OspA is the most important to understand.  OspA is band 31 on a western blot and it was the antigen of choice for the late (and not so great) vaccine. The western blot is measuring antibodies, so band 31 is the antibody that your body produces against OspA.

When you look at the structure of OspA, it is Pam3Cys.  A triacyl lipoprotein.

ospastructure

It has a tri-acyl (3 fatty acids) structure.  Pam3cys is a molecule that when inside the body it basically STOPS the typical immunity chain reaction and ends in immune suppression and immune tolerance.  Immune tolerance is when your body stops recognizing all kinds of pathogens. It’s basically an AIDS (ACQUIRED immune deficiency) in most of us. Pathogens that were once kept at bay by a healthy immune system now become rampant. They are called opportunistic infections because that’s what they do. They take the opportunity to attack due to a damaged immune response and wreak havoc in our bodies. Epstein-barr, the Herpes viruses like HHV-6, Parvo, Cytomegalovirus, systemic Candida, even cancer such as Lymphoma are some opportunistic pathogens.

     HIV-Aids affects the T cells while Lyme-Aids affects the B cells of the immune system.

Spirochetes shed (or bleb) their Osps as a way to evade to your immune cells.  So you have all these little lipoproteins floating around.  The blebs have the Osps on them.  Immune cells, like B cells, come along and eat these lipoproteins up. OspA and the other Osps are triacyl, which means FUNGAL (due to the fact that they are managed by TLRs 2 and 1), so when an immune cell eats this up it effectively turns the cell off and renders it useless.  Imagine an immune cell as a little ball  with little spiky things sticking out of it. The spiky things are called TLR’s which stand for Toll-Like Receptors.  The job they do is recognizing pathogens and telling everyone else about the invader.  They are all numbered 1, 2, 3, 4…..etc.

spirochetes shed highly acylated TLR2/1 agonists, turning off the immune system, AKA “Post-Sepsis Syndrome

spirochete with blebsOspA = pam3cys = unfixable immune suppression = immune tolerance to other pathogens = reactivated viruses + opportunistic pathogens = Post Sepsis Syndrome.  Life ruined.  Antibiotics can’t fix this.  EBV mostly causes the “Great Imitator” outcomes, think the likes of MS, ALS, etc .  No treatment because “Lyme disease” is only a bad knee. (More about this another day).

          OspA is a TLR 1/2 agonist. Which is exactly what it sounds like, bad.  Once an immune cell eats up these lipoproteins it is broken. More  IMPORTANTLY , Immune tolerance spreads to your other TLRs (cross-tolerance). All the different TLR’s recognize different stuff.  So TLR 1/2 deals with fungi, and humans just can’t take fungi. We say it is a fungal-like antigen because of what TLR manages it. Immune tolerance means that your immune system is broken in a very general sense.  It means that you can’t recognize or kill germs of all different kinds.So, now you have incompetent immune cells – almost like STUNNED or zombie  immune cells – floating around, because the Osps are fungal-ish or triacylated lipoproteins.  It is immune-suppressive because of what it does to your TLR’s; it creates cross-tolerance to other TLR’s.  So eventually its an AIDS outcome.  This damage is what CANNOT be fixed by standard ILADS treatments like antibiotics or herbal protocols.  It just won’t.  If patients initially feel better with these types of treatments?  Well, that’s anecdote.  Hearsay.  At best it’s just taking out whatever other pathogens they have and providing temporary relief.  Not the majority or we would have known about it by now and the mechanism for these cures would be published. Symptoms will naturally wax and wane anyway as spirochetes are Relapsing Fever organisms, and especially due to the opportunistics like mycoplasma and the reactivated herpesviruses.
Medvedev and Cross-Tolerance; Medvedev talking about Immunosuppression from Post-Lyme and Post-LYMErix Sepsis (TLR2-agonists or Pam3Cys is OspA or shed borrelial antigens)

IRAK4 kinase activity is not required for induction of endotoxin tolerance but contributes to TLR2-mediated tolerance

“Development of endotoxin tolerance following the initial “cytokine storm” phase of sepsis is thought to protect the host from an overexuberant immune response and tissue damage but at the same time, may render the host immunocompromised and more susceptible to secondary infection [18,–20]. …

“Reprogramming [21] of TLR4 signaling in endotoxin-tolerant monocytes and macrophages does not occur as a result of decreased TLR4 expression but involves altered recruitment, tyrosine phosphorylation, and K63-linked polyubiquitination of proximal receptor-adapter-kinase complexes [22,–27] and induction of negative regulators IRAK-M, SHIP1, and A20 [24, 25, 28]. Although a few studies have sought to dissociate kinase and adapter functions of IRAK4 in IL-1R/TLR signaling, albeit with conflicting results [13,–16, 29,–31], it is unclear how IRAK4 kinase activity affects induction of TLR2 and TLR4 homo- and heterotolerance. To address these questions, we used IRAK4KDKI mice to determine the impact of kinase deficiency of IRAK4 on the induction of TLR tolerance. Our data showed comparable induction of endotoxin tolerance in WT or IRAK4KDKI PMs and BMDMs, as judged by attenuated MAPK phosphorylation, inhibited expression of proinflammatory cytokines and chemokines, and up-regulation of negative TLR regulators, A20 and IRAK-M. Notably, IRAK4 kinase activity was found to be a prerequisite for conferring inhibition of LPS-inducible JNK and p38 MAPK activation following prior exposure to Pam3Cys. These results represent the first systematic analyses of the role of IRAK4 kinase activity in TLR homo- and heterotolerance and pave the way for improved understanding of how IRAK4 kinase dysregulation may underlie immunocompromised states in late sepsis.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714565/

Why call it Post-Sepsis Syndrome?

Due to the intense inflammatory response of the body caused by an infectious process, a phenomenon called endotoxin tolerance takes place in order to prevent acute organ failure and death.

“In response to tissue damage or an infection, innate immune cells will secrete many
inflammatory mediators to produce an inflammatory response. This occurs through innate cells, such as macrophages, due to the pattern recognition receptors (PRR) they possess on their surface. Toll-like receptor 4 (TLR4) is a member of the PRR family which is responsible for recognising gram-negative bacteria and their endotoxins, such as Lipopolysaccharide (LPS). This recognition allows the initiation of the inflammatory response that is firmly regulated throughout the immune system to prevent uncontrolled inflammation, which can lead to endotoxic shock, tissue damage and pathologies (Beutler, 2004).
The immune system has developed a defence mechanism against endotoxic shock thus preventing harmful pathologies like sepsis. Defined as a temporary hypo-responsiveness, endotoxin tolerance (ET) is known as one of these mechanisms (Ishiyama et al, 2006).
ET is characterised by a reduced production of cytokines when a pro-inflammatory stimulusis incurred. It occurs after an initial low dose of an endotoxin which renders the cell unresponsive when endotoxin is encountered for the second time(Biswas & Lopez-Collazo, 2009). This reduces the toxic effect of high levels of inflammatory mediators (Ishiyama et al, 2006).
“….immunosuppression that is present in sepsis has its purpose, which is to eliminate the significant proinflammatory activity initiated by the infectious agent….”

Immunotherapy of Sepsis: Blind Alley or Call for Personalized Assessment? (PDF Download Available). Available from: https://www.researchgate.net/publication/306431182_Immunotherapy_of_Sepsis_Blind_Alley_or_Call_for_Personalized_Assessment [accessed Aug 19, 2017].

“In a rapid and strong inflammatory response
such as during infections leading to sepsis, the role of adaptive
immunity might be lost due to the prompt development of events
plus the fact that their responses may be impaired due to the
profound depletion of T and B cells (68), leaving endotoxin
tolerance as the main mechanism to control inflammation.
Nevertheless, this suppressed-inflammatory/wound-healing state
would likely be dangerous if sustained for a prolonged period, as
the strong immunosuppression might lead to susceptibility to
secondary infections, increasing the risk of death.”

“Endotoxin tolerance protects the host by limiting excessive ‘cytokine storm’ during sepsis, but compromises the ability to counteract infections in septic shock survivors. It reprograms Toll-like receptor (TLR) 4 responses by attenuating the expression of proinflammatory cytokines without suppressing anti-inflammatory and antimicrobial mediators, but the mechanisms of reprogramming remain unclear. In this study, we demonstrate that the induction of endotoxin tolerance in human monocytes, THP-1 and MonoMac-6 cells inhibited lipopolysaccharide (LPS)-mediated phosphorylation of Lyn, c-Src and their recruitment to TLR4, but increased total protein phosphatase (PP) activity and the expression of protein tyrosine phosphatase (PTP) 1B, PP2A, PTP nonreceptor type (PTPN) 22 and mitogen-activated protein kinase phosphatase (MKP)-1. Chemical PP inhibitors, okadaic acid, dephostatin and cantharidic acid markedly decreased or completely abolished LPS tolerance, indicating the importance of phosphatases in endotoxin tolerization. Overexpression of PTPN22 decreased LPS-mediated nuclear factor (NF)-x03BA;B activation, p38 phosphorylation and CXCL8 gene expression, while PTPN22 ablation upregulated LPS-induced p65 NF-x03BA;B and p38 phosphorylation and the expression of TNF-α and pro-IL-1β mRNA, indicating PTPN22 as an inhibitor of TLR4 signaling. Thus, LPS tolerance interferes with TLR4 signaling by inhibiting Lyn and c-Src phosphorylation and their recruitment to TLR4, while increasing the phosphatase activity and expression of PP2A, PTPN22, PTP1B and MKP1.

© 2015 S. Karger AG, Basel.
http://www.ncbi.nlm.nih.gov/pubmed/26457672

          When they made the vaccine, LYMErix, they also made the disease. The disease is the vaccine the vaccine is the disease. That’s why a brave whistleblower came forward, that’s why it was really removed from the market! It’s not [LYME]! It really never was and if you look at the pre-1994 research by these same criminals you can read, ( in their own words ), what it was and STILL is!
          In 1994 in Dearborn, Michigan the diagnostic criteria for Relapsing Fever Borrelliosis [Lyme Disease], was changed.
FB_IMG_1446150501474

          Pam3Cys is the basic molecule of LYMErix or OspA and others shed by Borrelia:
A20 is critical for the induction of Pam3CSK4-tolerance in monocytic THP-1 cells.

“A20 functions to terminate Toll-like receptor (TLR)-induced immune response, and play important roles in the induction of lipopolysacchride (LPS)-tolerance. However, the molecular mechanism for Pam3CSK4-tolerance is uncertain. Here we report that TLR1/2 ligand Pam3CSK4 induced tolerance in monocytic THP-1 cells. The pre-treatment of THP-1 cells with Pam3CSK4 down-regulated the induction of pro-inflammatory cytokines induced by Pam3CSK4 re-stimulation. Pam3CSK4 pre-treatment also down-regulated the signaling transduction of JNK, p38 and NF-κB induced by Pam3CSK4 re-stimulation. The activation of TLR1/2 induced a rapid and robust up-regulation of A20, suggesting that A20 may contribute to the induction of Pam3CSK4-tolerance. This hypothesis was proved by the observation that the over-expression of A20 by gene transfer down-regulated Pam3CSK4-induced inflammatory responses, and the down-regulation of A20 by RNA interference inhibited the induction of tolerance. Moreover, LPS induced a significant up-regulation of A20, which contributed to the induction of cross-tolerance between LPS and Pam3CSK4. A20 was also induced by the treatment of THP-1 cells with TNF-α and IL-1β. The pre-treatment with TNF-α and IL-1β partly down-regulated Pam3CSK4-induced activation of MAPKs.

Furthermore, pharmacologic inhibition of GSK3 signaling down-regulated Pam3CSK4-induced A20 expression, up-regulated Pam3CSK4-induced inflammatory responses, and partly reversed Pam3CSK4 pre-treatment-induced tolerance, suggesting that GSK3 is involved in TLR1/2-induced tolerance by up-regulation of A20 expression. Taken together, these results indicated that A20 is a critical regulator for TLR1/2-induced pro-inflammatory responses.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3905037/

          TLR2/1-induced tolerance or LYMErix or Lyme tolerance is a thing, like Endotoxin Tolerance, only worse, since so far it is not reversible. In other words, IDSA and the CDC have no idea what they are talking about, and this concerns every major disease, if not every disease.        

          Patents had been bought and the process for controlling the outcome of the efficacy of a vaccine and the monopoly of Tick Borne Disease Testing was firmly in place. Rubbing their greedy hands together, they sat back and waited for the profits to come rolling in!
          I don’t know how that makes you feel? I know I’m really “ticked” off! I know I won’t stop speaking the TRUTH until these criminals are prosecuted and all involved are served JUSTICE. Then, and ONLY then, can research based on the TRUTH go forward. Only then can we receive care with dignity, with treatments that work and are covered by insurance.
          First, the TRUTH. Then, the CURE. WE must demand the DOJ prosecute the criminals!

 

 

 

 

 

 

 

 

 

 

     
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Published by

LiaBurgdorferi

RN for 24 years. Activist for TRUTH in Healthcare. Lyme Warrior. Battling this disease since the late 1980's

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