Lyme Crooks Finally Admit/Submit to LYMErix/Lyme Immunosuppression (Tufts)
Mort Zuckerman
lPick...@cdc.gov, Durlan...@yale.edu, Aa...@columbia.edu,
gary_w...@nymc.edu, scientifi...@ostp.gov,
pkru...@princeton.edu, Stanle...@fiu.edu,
margaret...@hhs.fds.gov, emcsw...@niaid.nih.gov,
afa...@niaid.nih.gov, Spin...@yahoogroups.com, kshe...@calea.org,
fit...@gmail.com, patrick.f...@usdoj.gov,
model...@sbcglobal.net, jdr...@nejm.org, let...@courant.com,
Jgerb...@cdc.gov, michae...@ct.gov, con...@po.state.ct.us,
executiv...@nytimes.com, managin...@nytimes.com, news-
ti...@nytimes.com, biz...@nytimes.com, for...@nytimes.com,
nati...@nytimes.com, dv...@cdc.gov, brigidc...@optonline.net,
tr...@hotmail.com, illino...@aol.com, jle...@courant.com,
tinaj...@yahoo.com, jhorn...@fff.org, thomas...@usdoj.gov,
thoma...@ct.gov, kur...@washpost.com, georg...@washpost.com,
p...@allegorypress.com, commissi...@po.state.ct.us,
brans...@comcast.net, vts...@comcast.net, o...@po.state.ct.us,
freet...@charter.net, scott....@po.state.ct.us,
govern...@po.state.ct.us, attorney...@ct.gov,
randall...@usdoj.gov, Robert....@yale.edu, editor@greenwich-
post.com, harol...@yale.edu, sedm...@nswbc.org, rrmcg...@aol.com,
fr...@nytimes.com, saint....@sbcglobal.netm, rre...@berkeley.edu,
pcal...@tribune.com
Cc: fra...@ucia.gov, dr-ahma...@president.ir,
eugener...@washpost.com, bmi...@newstimes.com, tr...@hotmail.com,
rast...@aol.com, billc...@gmail.com, amcg...@rms-law.com,
rjmu...@aol.com, paulcrai...@yahoo.com,
criminal...@usdoj.gov, karla.d...@usdoj.gov,
christophe...@usdoj.gov, richar...@yale.edu,
harol...@yale.edu, james.p...@yale.edu, inq...@aldf.com,
ly...@idsociety.org, meganm...@theatlantic.com
Subject: Lyme Crooks Finally Admit/Submit to LYMErix/Lyme
Immunosuppression (Tufts)
Date: Mar 11, 2011 5:40 AM
ARTICLE BELOW
===================================
Had to happen, cuz like I said on the homepage of ActionLyme.org, no
one can make a move unless they admit what LYMErix Is/Does:
http://www.actionlyme.org/
More Info (better and more accurate summary of the mechanisms of
immunosuppression/activation of latent common viruses than this,
below) at
http://www.actionlyme.org/101016.htm
This tosses Yale's/IDSA's "disease" (hypersensitivity-only) model and
the diagnostic standard for Lyme out the window, and with it,
Klempner's garbage and IDSA's downstream, "Lyme Causes Nothing"
insanity ("Guidelines on the Diagnosis and Treatment of Lyme Disease"
http://www.actionlyme.org/MKLEMPNER.htm
)
Now we're back to where we were in 1989, when IDSA published that
"Lyme is the New Great Imitator (causes MS, Lupus, ALS, Cancer, etc)":
http://www.actionlyme.org/CHP_9_IDSA_REVIEWS.htm
======================================
http://www.ncbi.nlm.nih.gov/pubmed/21387014
PLoS One. 2011 Feb 28;6(2):e17414.
Nod2 Suppresses Borrelia burgdorferi Mediated Murine Lyme Arthritis
and Carditis through the Induction of Tolerance.
Petnicki-Ocwieja T, Defrancesco AS, Chung E, Darcy CT, Bronson RT,
Kobayashi KS, Hu LT.
Division of Geographic Medicine and Infectious Diseases, Tufts Medical
Center, Boston, Massachusetts, United States of America.
Abstract
The internalization of Borrelia burgdorferi, the causative agent of
Lyme disease, by phagocytes is essential for an effective activation
of the immune response to this pathogen. The intracellular, cytosolic
receptor Nod2 has been shown to play varying roles in either enhancing
or attenuating inflammation in response to different infectious
agents. We examined the role of Nod2 in responses to B. burgdorferi.
In vitro stimulation of Nod2 deficient bone marrow derived macrophages
(BMDM) resulted in decreased induction of multiple cytokines,
interferons and interferon regulated genes compared with wild-type
cells. However, B. burgdorferi infection of Nod2 deficient mice
resulted in increased rather than decreased arthritis and carditis
compared to control mice. We explored multiple potential mechanisms
for the paradoxical response in in vivo versus in vitro systems and
found that prolonged stimulation with a Nod2 ligand, muramyl dipeptide
(MDP), resulted in tolerance to stimulation by B. burgdorferi. This
tolerance was lost with stimulation of Nod2 deficient cells that
cannot respond to MDP. Cytokine patterns in the tolerance model
closely paralleled cytokine profiles in infected Nod2 deficient mice.
We propose a model where Nod2 has an enhancing role in activating
inflammation in early infection, but moderates inflammation after
prolonged exposure to the organism through induction of tolerance.
KMDickson