Format

Send to

Choose Destination
See comment in PubMed Commons below
PLoS Curr. 2013 Dec 13;5. pii: ecurrents.hd.5791c897b5c3bebeed93b1d1da0c0648. doi: 10.1371/currents.hd.5791c897b5c3bebeed93b1d1da0c0648.

JAK/STAT Signalling in Huntington's Disease Immune Cells.

Author information

1
Department of Neurodegenerative Disease, Institute of Neurology, University College London, London, UK.
2
Department of Experimental Medical Science, Wallenberg Neuroscience Center, Lund University, Lund, Sweden.
3
University College London, London, UK.
4
Institute of Neurology, University College London, London, UK; Bristol University, Bristol UK.

Abstract

Huntington's disease (HD) is an inherited neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin (HTT) gene. Both central and peripheral innate immune activation have been described as features of the disease. Isolated human HD monocytes have been shown to produce more cytokines upon LPS stimulation compared to control monocytes. Understanding alterations in the signalling cascades responsible and activated by this increase in pro-inflammatory cytokine production is crucial in understanding the molecular basis of this phenomenon. Here we investigated the signalling cascade most commonly activated by pro-inflammatory cytokines such as IL-6 - the JAK/STAT signalling cascade. Using flow cytometry, we show that one out of three key transcription factors activated by JAK/STAT signalling is altered in primary human HD innate immune cells, suggesting that this pathway may only play a minor, additive role in the immune cell dysfunction in HD.

PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Support Center