Steere himself undoes the theory that "all diseases are a result of inflammation"
Mort Zuckerman
lPick...@cdc.gov, Durlan...@yale.edu, Aa...@columbia.edu,
gary_w...@nymc.edu, scientifi...@ostp.gov,
pkru...@princeton.edu, Stanle...@fiu.edu,
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...@po.state.ct.us, con...@po.state.ct.us, executive-
edi...@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...@po.state.ct.us, 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...@po.state.ct.us, randall...@usdoj.gov,
Robert....@yale.edu, edi...@greenwich-post.com,
harol...@yale.edu, sedm...@nswbc.org, rrmcg...@aol.com,
fr...@nytimes.com, dpr...@stmartin.edu, saint....@sbcglobal.net
Cc: fra...@ucia.gov, dr-ahma...@president.ir,
eugener...@washpost.com, afa...@niaid.nih.gov,
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: Steere himself undoes the theory that "all diseases are a
result of inflammation"
Date: May 28, 2010 11:53 AM
I better leave Corrupticut soon -
Before I die (laughing)!
Immune Suppression even in Lyme
arthritis patients:
http://www.ncbi.nlm.nih.gov/pubmed/2050631
Arthritis Rheum. 2010 Mar 26. [Epub ahead of print]
T regulatory cell numbers and function in patients with antibiotic-
refractory or antibiotic-responsive lyme arthritis.
Shen S, Shin JJ, Strle K, McHugh G, Li X, Glickstein LJ, Drouin EE,
Steere AC.
Harvard Medical School and Massachusetts General Hospital, Boston,
Massachusetts.
Abstract
OBJECTIVE.: In a murine model of antibiotic-refractory Lyme arthritis,
the numbers of T regulatory cells (Treg) are dramatically reduced. Our
goal was to examine Treg numbers and function in human patients with
antibiotic-refractory Lyme arthritis. METHODS.: CD4+ T cell subsets
were enumerated in peripheral blood (PB) and synovial fluid (SF) in 12
patients with antibiotic-refractory arthritis and 6 with antibiotic-
responsive arthritis. Treg function was examined using Borrelia-
specific and non-specific Treg proliferation assays. RESULTS.: In both
patient groups, IFN-gamma+ T(H)1 cells in SF were abundant and
enriched ( approximately 50% of CD4+ T cells). In patients with
antibiotic-refractory arthritis, the median percentages of FoxP3+ Treg
were significantly higher in SF than PB (12% versus 6%) (P<0.01) or in
SF in patients with antibiotic-responsive arthritis (12% versus 5%)
(P=0.04). Moreover, in the refractory group, a higher percentage of
Treg in SF correlated with a shorter duration to resolution of
arthritis (r = -0.74, P = 0.006). In contrast, patients with fewer
Treg had suboptimal responses to DMARDs and longer duration of
arthritis after antibiotics, and they often required synovectomies for
arthritis resolution. In each group, Treg in SF dampened B.
burgdorferi-specific proliferative responses, and in 2 patients with
refractory arthritis, Treg were functional in non-specific suppression
assays. CONCLUSIONS.: Treg were functional in patients with antibiotic-
refractory arthritis, and in some patients, higher numbers of these
cells in SF appeared to participate in arthritis resolution. However,
as in the murine model, patients with refractory arthritis and lower
numbers of Treg seemed unable to resolve synovial inflammation.
PMID: 20506317 [PubMed - as supplied by publisher]
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci