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in case you missed it....
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eugeneshapiroisapig
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Joined: 24 Mar 2005
Posts: 2108

PostPosted: Wed Jun 28, 2006 2:06 am    Post subject: in case you missed it.... Reply with quote

Borrelia burgdorferi Induces TLR1 and TLR2 in Human Microglia and
Peripheral Blood Monocytes but Differentially Regulates HLA-Class II
Expression.

Cassiani-Ingoni R, Cabral ES, Lunemann JD, Garza Z, Magnus T,
Gelderblom H, Munson PJ, Marques A, Martin R.

Quote:
From the Cellular Immunology Section (RCI, ESC, JDL, HG, RM),
Neuroimmunology Branch, National Institute of Neurological Disorders

and Stroke, Bethesda, Maryland; Mathematical and Statistical Computing
Laboratory (ZG, PJM), Analytical Biostatistics Section, Center for
Information Technology, Bethesda, Maryland; Stem Cell Biology Unit
(TM), Laboratory of Neuroscience, National Institute on Aging,
Bethesda, Maryland; Laboratory of Clinical Infectious Diseases (AM),
National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Bethesda, Maryland; and Department of Human
Physiology and Pharmacology (RCI), Center of Excellence in Biology and
Molecular Medicine, University of Rome "La Sapienza," Rome, Italy.

The spirochete Borrelia burgdorferi is the agent of Lyme disease, which
causes central nervous system manifestations in up to 20% of patients.
We investigated the response of human brain microglial cells, glial
progenitors, neurons, astrocytes, as well as peripheral blood monocytes
to stimulation with B. burgdorferi. We used oligoarrays to detect
changes in the expression of genes important for shaping adaptive and
innate immune responses. We found that stimulation with B. burgdorferi
lysate increased the expression of Toll-like receptors (TLRs) 1 and 2
in all cell types except neurons. However, despite similarities in
global gene profiles of monocytes and microglia, only microglial cells
responded to the stimulation with a robust increase in HLA-DR, HLA-DQ,
and also coexpressed CD11-c, a dendritic cell marker. In contrast, a
large number of HLA-related molecules were repressed at both the RNA
and the protein levels in stimulated monocytes, whereas secretion of
IL-10 and TNF-alpha was strongly induced. These results show that
signaling through TLR1/2 in response to B. burgdorferi can elicit
opposite immunoregulatory effects in blood and in brain immune cells,
which could play a role in the different susceptibility of these
compartments to infection.
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