“Thus, it is of interest to consider potential roles for the inhibition of the CP beyond protection from complement-mediated attack. For example, upon colonizing lymph tissue B. burgdorferi disrupts the normal formation of germinal centers (GC) [60,61]. Lack of normal GC development ultimately results in reduced antibody titers against B. burgdorferi in experimental infection . Local complement C4 deposition on follicular dendritic cells (FDC) is significantly reduced in B. burgdorferi infected lymph nodes and this is speculated to be responsible for the premature collapse of GC responses due to diminished antigen presentation by FDCs .”
“Local complement C4 deposition on follicular dendritic cells (FDC) is significantly reduced in B. burgdorferi infected lymph nodes and ***this is speculated to be responsible for the premature collapse of GC responses due to diminished antigen presentation by FDCs ***…”
Here is what Baumgarth said, most recently:
“By decreasing the capacity of the host to produce effective antibodies against B. burgdorferi, the GC collapse may help B. burgdorferi evade clearance. The signals and mechanisms leading to the collapse, however, are unknown. One possible mechanism is the interference of B. burgdorferi with the complement system. Continued antigen presentation is crucial for hyperaffinity maturation, and components of the complement system are known to be involved in this process. Specifically, activated C3 and C4 fragments bound to antigen and adhere to complement receptors 1 and 2 (CR1 and CR2). These receptors are present on the major antigen-presenting cells in the GC, the FDC, and on GC B cells. It was shown previously that GCs will form normally in mice lacking CR1 and CR2, but collapse prematurely, before GCs can perform their important functions (120). This phenotype is strikingly similar to that seen in wild-type mice infected with B. burgdorferi. Interestingly, in B. burgdorferi-infected mice, although CR1 and CR2 are present on FDCs and GC B cells, C4 is not detectable (69). C4 is typically deposited on the surface of FDCs supporting antigen presentation. Interference with C4 deposition could inhibit antigen presentation by FDCs to GC B cells and thereby lead to GC collapse. B. burgdorferi interference with activation of complement could also have various indirect effects on GCs: changing the cytokine milieu, reducing antigen presentation to naïve B cells via CR1 on APCs outside the GC, reducing naïve B cell activation viaco-stimulation with CR2, and reducing opsonization (and thus uptake) of antigens. Exploring the role of complement and complement inhibition by B. burgdorferi during infection are important subjects for future studies.”
Of course there is another reason antigen is not presented – it could be OspA, or Pam3Cys, which downregulates that function.
Previously, (posted Dec 2016):
HOW could it be surprising that the U.S. Govt. is lying about “Lyme disease,” if everyone knows they’ve already done this?
White people are known to be more susceptible to dementia from borrelia or syphilis – and this was the reason for the Tuskegee and Guatemala syphilis crimes:
Toll-like Receptor Polymorphisms Are Associated with Increased Neurosyphilis Risk
“Clinicians in the early 20th century posited that race influenced susceptibility to neurosyphilis, citing a decreased risk in African Americans compared to Caucasians (7). Subsequent work suggested a genetic basis for such differences, with an increased risk of syphilitic dementia, but not other forms of neurosyphilis, in patients with certain HLA types (8) that differed in African Americans compared to Caucasians (9). While more recent reports suggest that there may be genetic contributions to syphilis susceptibility (10-13), to the best of our knowledge there have been no recent investigations of genetic susceptibility to neurosyphilis.”
Spirochetes ruin your immune system by “stealth bombing” (Barthold and Barbour) it with blebs that have fungal lipoproteins on them and DNA in them (Dorward, discussed around 1990, and also discussed at the LDF conferences in NYC in the late 1990s which I attended). The reactivation of latent viruses, basically is what drives the chronic fatiguing disease (opportunistics, or the result of TOLERANCE and cross-tolerance).
See for yourselves, Dorward, NIH, RML:
What is the process by which spirochetes damage B cell germinal centers (Baumgarth, Barthold http://ccm.ucdavis.edu/our-science/lyme-borreliosis/) would be what we want to know next. Is it the shed blebs that contain DNA, or is it like Steere (HLA connection), Paul Duray, & Dave Persing (“Target Imbalance”) describe what they see in “bad knees” (shed exosomes outnumber spirochetes, sticking to everything)?
Here we have a report that ties in the relatedness of several diseases (Occam’s Razor, below), and what is the official Govt spin (Victim-Blaming) But the head of NIAID owns a patent for this very-, officially-denied-, condition we call Lyme or CFIDS or Fibro. There is no OPPOSITE of “ALLERGY” or HLA-linked hypersensitvity or autoimmunity “National Institute of…”.
If you dont know what “HLA-linked autoimmunity” means, look that up now.
The U.S. Govt does not recognize chronic illnesses that are not-HLA-linked – which includes the majority of vaccine-autism cases as well as is the very foundation of the science of “stealth disablers” (fungal-ish animal diseases that leave no antibody trace of the original infection, but which “overwhelm the immune system”).
The U.S. Govt. has clearly twice before experimented with spirochetes as disablers of the immune system: Tuskegee and Guatemala (native Americans). China also claims USA dropped Borrelia on them, too, found in bugs suddenly appearing in the winter, on the snow, which would not be expected. Therefore what Korea claimed about Americans’ war crimes may have been true.
When the US Navy descended upon Unit 731 in Manchuria at the end of World War II, among the organisms they found and brought back home was Brucella, a “lameness” causing illness that bears LYMErix-like antigens. So much for the “phage-vectored DNA” or “Lateral Gene Transfer” (plasmids) that I have been talking about since at least 2001 (Albany Lyme hearing, November).
Edward McSweegan worked for the US Navy and stole their vector- borne diseases funding via a fake whistleblower letter to Senator Goldwater in 1986, the DNA patenting era (Dole-Bayh Act). Then he was put in charge of the NIAID TBDs grants, funneling them into his own particular criminal outlaw gang, including Durland Fish and CDC officers Johnson and Barbour, called the ALDF, which ws founded in 1990, a year after Pat Smith’s LDA.
This criminal racketeering enterprise, ALDF.com, changed the Lyme case definition to exclude the fungal-related immunosuppression outcomes to spirochetes because they could not otherwise sell vaccines and test kits based on their own patented DNA.
But here you see…
The most serious form of Lyme, neurologic or chronic neurologic, will have no antibodies against the Outer Surface Proteins, since they’re fungal, TLR2/1 agonists and cause tolerance which is a form of immunosuppression. Above, you see Allen Steere say all this plainly. The people with the chronic neurological outcome of Lyme, will not test positive to the arthritis-only case definition, we refer to as “Dearborn.”
They, this criminal ALDF RICO organisation, at the same time proceeded to attack MDs like Joe Burrascano and others (many activists, including the LDF) who claim spirochetal diseases were long term infections and not cured with short term antibiotics. Finally in early 1999 when their fake OspA vaccine hit the market, it was giving people “Lyme again.” This was overwhelmingly puzzling… since it was a recombinant ANTIGEN, and not whole spirochetes. Some of the ALDF members were CDC officers. Such aggression is known as “Color of Law” abuses.
That there are Lyme disease “guidelines” based on this fraud, published by IDsociety.org, based on the Dearborn case definition, means this federal charge is still viable against all the signers of the “guidelines.”