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Subject: Spirochetal Immunosuppression in Otherwise-Peridontitis
Date: Oct 31, 2009 10:19 AM
ARTICLE BELOW
==============================
Yes, we know. Thank you:
http://www.actionlyme.org/Pam3Cys_Version15.htm
Spirochetal, Tuberculosis, and HIV complex
(Pam3Cys; TLR2 agonists) lipids suppress the
immune response.
Had the Lyme criminals been honest about
it, here, too, in dental health, there
would have been scientific progress.
This Lymecryme negatively affected research
in EVERY disease.
People with bad gums tend to have
arthritis, too. You know, like if
you tested positive to Steere's Lyme
HLA:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC280920/?tool=pubmed
standard, you would have arthritis *and*
bad gums:
http://www.perio.org/consumer/arthritis.htm
But, you see, bad gums and arthritis is
*NOT* a character flaw, whereas Multiple
Sclerosis *is* a character flaw.
Just ask Roland Martin:
http://www.actionlyme.org/MARTIN_NINDS_MS_CHRONIC_LYME.htm
"As an example for the latter, our data for organ-infiltrating T cells
in chronic nervous system Lyme disease already suggest that the immune
response in the chronic stage of the disease is directed against
tissue autoantigens and that this process is thus very similar to an
autoimmune disease."
Autoimmune Laquapeniitis.
KMDickson
==========================================
http://www.ncbi.nlm.nih.gov/pubmed/19596768?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=4
2009 Sep;77(9):3939-47. Epub 2009 Jul 13.
Involvement of Toll-like receptors 2 and 4 in the innate immune
response to Treponema denticola and its outer sheath components.
Nussbaum G, Ben-Adi S, Genzler T, Sela M, Rosen G.
Institute of Dental Sciences, Faculty of Dental Medicine, Hadassah and
Hebrew University Medical Center, Jerusalem, Israel.
gabrieln at (no spam) ekmd.huji.ac.il
Treponema denticola is considered an important oral pathogen in the
development and progression of periodontal diseases. In the present
study, the mechanisms of recognition and activation of murine
macrophages by T. denticola and its major outer sheath protein (MSP)
and lipooligosaccharide (LOS or glycolipid) were investigated. T.
denticola cells and the MSP induced innate immune responses through
TLR2-MyD88, whereas LOS induced a macrophage response through TLR4-
MyD88. The presence of gamma interferon (IFN-gamma), or of high
numbers of T. denticola, circumvented the requirement for TLR2 for the
macrophage response to T. denticola, although the response was still
dependent on MyD88. In contrast, synergy with IFN-gamma did not alter
the TLR dependence of the response to the T. denticola surface
components LOS and MSP, despite enhanced sensitivity. These data
suggest that although there is flexibility in the requirements for
recognition of T. denticola cells (TLR2 dependent or independent),
MyD88 is a requirement for the downstream signaling events that lead
to inflammation. We also demonstrate that both outer sheath molecules
LOS and MSP induce macrophage tolerance to further stimulation with
enterobacterial lipopolysaccharide. Tolerance induced by T. denticola
components during mixed infections may represent a general mechanism
through which bacteria evade clearance.
PMID: 19596768 [PubMed - indexed for MEDLINE]
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci |
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