Another mechanism of OspA-induced immunosuppression published
Mort Zuckerman
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Subject: Another mechanism of OspA-induced immunosuppression published
Date: Apr 16, 2010 9:08 AM
Okay. I'll add that to the list
of HIV/Tuberculosis/Fungal immunosuppression
mechanisms not identified by Yale or UConn
http://www.actionlyme.org/Pam3Cys_Version15.htm
because they decided to lie about LYMErix
in 1994 (Schoen, Steere, and Persing):
http://www.actionlyme.org/CORIXARICO.htm
(the little secret mini-cabal who knew
LYMErix caused chronic, neurologic Lyme-
like symptoms).
1994:
http://www.actionlyme.org/Dearborn_Who_Approved.htm
^^^Barbour, McSweegan, Steere, CDC's Barbara
Johnson, and Arthur Weinstein.
http://www.actionlyme.org/ARTHURWEINSTEIN.htm
1991:
http://www.actionlyme.org/SV_PPT_2_files/v3_document.htm
Kathleen M. Dickson
http://www.relapsingfever.org
http://www.actionlyme.org
=============================
http://www.ncbi.nlm.nih.gov/pubmed/20393136
J Immunol. 2010 Apr 14. [Epub ahead of print]
TLR2 Utilization of Borrelia Does Not Induce p38- and IFN-{beta}
Autocrine Loop-Dependent Expression of CD38, Resulting in Poor
Migration and Weak IL-12 Secretion of Dendritic Cells.
Hartiala P, Hytönen J, Yrjänäinen H, Honkinen M, Terho P, Söderström
M, Penttinen MA, Viljanen MK.
Department of Medical Microbiology and Immunology.
Abstract
Lyme borreliosis is a tick-borne bacterial infection that in many
cases is limited to the skin. However, in some patients the bacterium
evades the immune response and disseminates into various organs.
Dendritic cells (DCs) are among the first cells to meet invading
pathogens in the skin. We have previously shown that CD38, an
ectoenzyme involved in the migration of DCs and generally upregulated
by microbial stimuli, is not upregulated in Borrelia garinii-
stimulated DCs. In this paper, we characterize the cellular events
that lead to the absence of CD38 on the DC surface after B. garinii
stimulation and investigate the consequences of absent CD38 expression
for the migration of DCs in vitro and in vivo. The data show that 1)
effective signaling via p38 MAPK (and STAT1 and NF-kappaB) is needed
for CD38 expression and ***2) TLR2 stimulation [OspA]
http://www.actionlyme.org/Pam3Cys_Version15.htm
, as opposed to TLR4 stimulation, ***does not induce*** IFN-beta
autocrine loop-dependent expression of CD38 and secretion of IL-12.
Further, we show that 3) B. garinii-stimulated DCs ***do not
migrate*** effectively toward CCL19 and CCL21 and 4) after B. garinii
infection of mice, the number of DCs migrating from the infection site
to draining lymph nodes is ***only half*** that induced by Escherichia
coli infection. Our results provide evidence for the first time that
different TLR use results in different CD38 expression, which
correlates with the migratory potential of DCs.
PMID: 20393136 [PubMed - as supplied by publisher]
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