Response of Toll-like receptors in experimental Guillain-Barré syndrome: a kinetic analysis

Neuroscience Letters
Manuela GriesSilke Walter

Abstract

Guillain-Barré syndrome (GBS) is an autoimmune disorder caused by the interaction between cellular and humoral immune responses in the peripheral nervous system. Toll-like receptors (TLRs) are key players in innate and have regulatory functions in adaptive immunity. In this study, we systematically examined expression patterns of TLRs in sciatic nerve and lymphoid organs during the disease course of murine experimental autoimmune neuritis and in blood from Guillain-Barré patients. A kinetic response pattern was identified, characterized by a pronounced up-regulation of TLR2, 6 and 11 on T cells and TLR4 and 6 on APCs, while TLR1 expression was decreased. Moreover, an enhanced expression of the disease promoting cytokine Interleukin-(IL)17A was detected. Additional analysis of GBS patients revealed an up-regulation of TLR2, TLR4 and TLR6 mRNA, negatively correlated with disease severity. This first systematic analysis of TLR expression pattern may contribute to elucidating the role of TLRs in GBS pathophysiology.

References

Jun 15, 2006·Journal of Neuropathology and Experimental Neurology·Marcus MüllerReinhard Kiefer
Jul 27, 2007·European Journal of Immunology·Ralf R Schumann, Richard I Tapping
Jan 19, 2008·European Journal of Immunology·Monica MartaAnna Lobell
Apr 23, 2008·Allergology International : Official Journal of the Japanese Society of Allergology·Toshimasa Aranami, Takashi Yamamura
Apr 25, 2008·Neuroimmunomodulation·Yong-Ning Deng, Wen-Bin Zhou
Feb 12, 2009·Neuropathology and Applied Neurobiology·Z-Y ZhangH J Schluesener
Nov 10, 2011·Neuroimmunomodulation·Yu-Zhong WangHuan Yang

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Citations

Apr 1, 2014·Journal of Neuroinflammation·Mark StettnerBernd C Kieseier
May 29, 2015·Annals of Neurology·Ruth HuizingaBart C Jacobs
Jun 21, 2013·Journal of the Peripheral Nervous System : JPNS·Simon Rinaldi
Jan 24, 2015·Mediators of Inflammation·Kishan Kumar Nyati, Kashi Nath Prasad

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