Maybe the genius and "Leader," Anthony Fauci, can tell us why...
Mort Zuckerman
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Subject: Maybe the genius and "Leader," Anthony Fauci, can tell us
why...
Date: Jan 3, 2010 3:42 AM
Gee, Ton,
What's the connection between HLA-linked
hypersensitivity to mycoplasmal lipoproteins
(Steere's knees and asthma), and the downregulation
of TLR2? And the downregulation of TLR2 and
Epstein-Barr running rampant in Pam3Cys
(mycoplasmal lipoproteins) tolerance?
(BELOW)
I'm so confused.
Well, at least it's clear that hypersensitity
to mycoplasma is an established cause of
asthma. But we don't talk about the
other extreme end of responses to these
antigens, do we? Because that hits too
close to home when talking about molds-
(airborne fungi and HIV-vaccine-like-
immunosuppression) and the hypervaccination
of children with "Autism" or inflammation of
the brain from not-attentuated-enough, ie.,
DEAD viral vaccines.
Huh?
Is this the reason there is no National
Institute of Immune Suppression Disorders
to go with your patented treatment of
Immune Suppression Disorders?
http://www.actionlyme.org/MKLEMPNER.htm
Huh?
"The methods of the present invention can be effective against disease
states in which IL-2 plays a role in the associated immune response.
The targeted disease state can comprise, for instance, an infection of
the patient by a pathogen against which a cellular immune response is
the principal mechanism for specific immunity therefor in the patient,
such as viral infections. See Abbas et al., CELLULAR AND MOLECULAR
IMMUNOLOGY 309-10 (W. B. Saunders Co., Philadelphia 1991).
***Illustrative of specific disease states in treatment of which the
present invention can be applied are HIV infection and other diseases
characterized by a decrease of T-cell immunity, for example,
mycobacterial infections like tuberculosis and fungal infections such
as cryptococcal disease. This method also can be used in the treatment
of secondary infections that occur in patients with suppressed immune
systems, such as the opportunistic infections that occur in AIDS
patients.***
'Like MS or Lyme-MS or what did the CDC
used ta call it?
"Chronic Meningitis from Chronic Lyme
or Relapsing Fever."
Right, Ton'?
KMDickson
http://www.actionlyme.org
====================================
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed&uid=18202345&ordinalpos=1&log$=relatedarticles&logdbfrom=pubmed
Am J Respir Crit Care Med. 2008 Apr 1;177(7):720-9. Epub 2008 Jan 17.
Toll-like receptor 2 down-regulation in established mouse allergic
lungs contributes to decreased mycoplasma clearance.
Wu Q, Martin RJ, Lafasto S, Efaw BJ, Rino JG, Harbeck RJ, Chu HW.
National Jewish Medical and Research Center, 1400 Jackson Street, Room
A639, Denver, CO 80206, USA. ch...@njc.org
RATIONALE: Respiratory Mycoplasma pneumoniae (Mp) infection is
involved in asthma pathobiology, but whether the established allergic
airway inflammation compromises lung innate immunity and subsequently
predisposes patients with asthma to Mp infection remains unknown.
Objectives: To test whether the established allergic airway
inflammation compromises host innate immunity (e.g., Toll-like
receptor 2 [TLR2]) to hinder the elimination of Mp from the lungs.
METHODS: We used mouse models of ovalbumin (OVA)-induced allergic
airway inflammation with an ensuing Mp infection, and cultures of
mouse primary lung dendritic cells (DCs) and bone marrow-derived DCs.
MEASUREMENTS AND MAIN RESULTS: Lung Mp clearance in allergic mice and
TLR2 and IL-6 levels in lung cells, including DCs as well as cultured
primary lung DCs and bone marrow-derived DCs, were assessed. The
established OVA-induced allergic airway inflammation, or the prominent
Th2 cytokines IL-4 and IL-13, inhibited TLR2 expression and IL-6
production in lung cells, including lung DCs, and eventually led to
impaired host defense against Mp. Studies in IL-6 knockout mice
indicated that IL-6 directly promoted Mp clearance from the lungs.
IL-4- and IL-13-induced suppression of TLR2 was mediated by inhibiting
nuclear factor-kappaB activation through signal transducer and
activator of transcription 6 (STAT6) signaling pathway. CONCLUSIONS:
The established OVA-induced allergic airway inflammation impairs TLR2
expression and host defense cytokine (e.g., IL-6) production, and
subsequently delays lung bacterial clearance. This could offer novel
therapeutic strategies to reinstate TLR2 activation by using TLR2
ligands and/or blocking IL-4 and IL-13 to ameliorate persisting
respiratory bacterial infections in allergic lungs.
PMID: 18202345 [PubMed - indexed for MEDLINE]
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci