New: How LYMErix causes Seronegative Lyme/Great Imitators/LYMErix Disease (CV Harding)
Mort Zuckerman
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Subject: New: How LYMErix causes Seronegative Lyme/Great Imitators/
LYMErix Disease (CV Harding)
Date: Jul 30, 2010 10:01 AM
More proof that Yale, NYMC,
the CDC, the NIH, the AMA and
the Infectious Diseases Society of
Israel (sued by AG Blumenthal for
FRAUD) don't know what the hell
they're talking about; be it HIV,
Tb or Relapsing Fever:
ALL:
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Harding%20CV%22[Author]
NEW:
http://www.ncbi.nlm.nih.gov/pubmed/20660347
J Immunol. 2010 Jul 21. [Epub ahead of print]
Mycobacterium tuberculosis and TLR2 Agonists Inhibit Induction of Type
I IFN and Class I MHC Antigen Cross Processing by TLR9.
Simmons DP, Canaday DH, Liu Y, Li Q, Huang A, Boom WH, Harding CV.
Department of Pathology.
Abstract
Dendritic cells (DCs) cross process exogenous Ags and present them by
class I MHC (MHC-I) molecules to CD8(+) T cells specific for Ags from
viruses and bacteria such as Mycobacterium tuberculosis. Unmethylated
CpG DNA signals through TLR9 to induce type I IFN (IFN-alpha/beta),
which enhances MHC-I Ag cross processing, but lipoproteins that signal
through TLR2 do not induce IFN-alpha/beta. In these studies we
observed that M. tuberculosis, which expresses agonists of both TLR9
and TLR2, did not induce production of IFN-alpha/beta or cross
processing by murine DCs. Furthermore, M. tuberculosis and TLR2
agonists inhibited induction of IFN-alpha/beta and DC cross processing
by CpG DNA. Exogenous IFN-alpha/beta effectively enhanced cross
processing of M. bovis bacillus Calmette-Guérin expressing OVA,
bypassing the inhibition of induction of endogenous IFN-alpha/beta. In
addition, inhibition of TLR9-induced cross processing of M. bovis
bacillus Calmette-Guérin expressing OVA could be circumvented by
pretreating cells with CpG DNA to induce IFN-alpha/beta and MHC-I
cross processing before inhibitory mycobacterial TLR2 agonists were
present. Inhibition of the response to one TLR by another may affect
the ultimate response to pathogens like M. tuberculosis that express
agonists of multiple TLRs, including TLR2 and TLR9. This mechanism may
contribute to immune evasion and explain why IFN-alpha/beta provides
little contribution to host immunity to M. tuberculosis. However,
downregulation of certain TLR responses may benefit the host by
preventing detrimental excessive inflammation that may occur in the
presence of persistent infection.
http://www.actionlyme.org
http://www.relapsingfever.org
KMDickson