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J Neuroinflammation. 2013 Jun 21;10:74. doi: 10.1186/1742-2094-10-74.

Impaired toll-like receptor 8 signaling in multiple sclerosis.

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  • 1Section of Infections of the Nervous System, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bldg 10, 7C-103, 10 Center Drive, Bethesda, MD 20892, USA.



The etiology and immunopathology of multiple sclerosis (MS) is not well understood. It is recognized that although autoreactive T cells are the main early mediators of disease, other cell types, including cells of the innate immune system contribute to MS pathogenesis. The objective of this study was to determine if Toll-like receptor (TLR) signaling is functionally altered in patients with MS.


Peripheral blood mononuclear cells from healthy donors and patients with relapsing remitting MS were stimulated with specific agonists of TLRs 3, 7, 8 and 9. Using quantitative polymerase chain reaction transcript levels of tumor necrosis factor-α, interferon-α and interleukin (IL)-12β were quantified from patients with MS and healthy donors. TLR8-induced production of IL12B transcripts and protein was functionally impaired in patients with MS as compared to healthy controls (P <0.05 and P <0.005, respectively). Patients with MS also expressed lower baseline levels of TLR8 as compared to healthy controls (P <0.05).


TLR8 expression and signaling is impaired in peripheral blood mononuclear cells from patients with MS. This finding suggests that loss of TLR8 signaling may be contributing to autoimmune processes in MS.

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