DOWNLOAD THE FULL TEXT of Dattwyler talking about seronegative, neuroLyme,
Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte
responses to Borrelia burgdorferi.
Department of Medicine, State
University of New York, School of
Medicine, Stony Brook 11794-8161.
The diagnosis of Lyme disease often
depends on the measurement of serum
antibodies to Borrelia burgdorferi,
the spirochete that causes this
disorder. Although prompt treatment
with antibiotics may abrogate the
antibody response to the infection,
symptoms persist in some patients.
We studied 17 patients who had
presented with acute Lyme disease
and received prompt treatment with
oral antibiotics, but in whom
chronic Lyme disease subsequently
developed. Although these patients
had clinically active disease, none
had diagnostic levels of antibodies
to B. burgdorferi on either a
standard enzyme-linked immunosorbent
assay or immunofluorescence assay.
On Western blot analysis, the level
of immunoglobulin reactivity against
B. burgdorferi in serum from these
patients was no greater than that in
serum from normal controls. The
patients had a vigorous T-cell
proliferative response to whole B.
burgdorferi, with a mean ( +/- SEM)
stimulation index of 17.8 +/- 3.3,
similar to that (15.8 +/- 3.2) in 18
patients with chronic Lyme disease
who had detectable antibodies. The
T-cell response of both groups was
greater than that of a control group
of healthy subjects (3.1 +/- 0.5; P
less than 0.001). We conclude
that the presence of chronic Lyme
disease cannot be excluded by the
absence of antibodies against B.
burgdorferi and that a specific
T-cell blastogenic response to B.
burgdorferi is evidence of infection
in seronegative patients with
clinical indications of chronic Lyme
[◄Note that I mention to the 2001 LYMErix FDA Vaccine Committee (which
Dattwyler was on) this NK cell immunosuppression, in addition to mentioning
that it was known that OspA
activates the anti-inflammatory cytokine IL-10
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