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AMERICAN SOCIETY FOR NEUROCHEMISTRY The Latest in Molecular and Cellular Neurobiology
Editorial Board
Monica Carson
  Riverside, U.S.A.

Deputy Editor-in-Chief
Christopher S. Colwell
  Los Angeles, U.S.A.

Reviews Editors
Scott T. Brady
  Chicago, U.S.A.
Wilma J. Friedman
  Newark, U.S.A.

Senior Editors
Susan Y. Bookheimer
  Los Angeles, U.S.A.
Carol A. Colton
  Durham, U.S.A.
Iryna M. Ethell
  Riverside, U.S.A.
Kazuhiro Ikenaka
  Osaka, Japan
Wendy Macklin
  Denver, U.S.A.
Mary C. McKenna
  Baltimore, U.S.A.
Vladimir Parpura
  Birmingham, U.S.A.
Thomas Seyfried
  Chestnut Hill, U.S.A.

Founding Editor
Anthony T. Campagnoni
  Los Angeles, U.S.A.
ISSN: 1759-0914
Published by Portland Press Limited on behalf of the American Society for Neurochemistry
*Publication time subject to receipt of payment
†2012 Journal Citation Reports® (Thomson Reuters, 2013)

Welcome to the NEURO Immunity knowledge environment!

The NEURO Immunity knowledge environment welcomes research on autoimmunity, CNS-pathogen interactions, immune privilege, immune suppression, immune-based therapies, inflammation, neuro-immune interactions, neuroinflammatory disorders, PAMP and DAMP receptors.
Accepted papers - IMPS
45th Annual ASN Meeting
Long Beach, California, 8-12 March 2014
Sölden Austria, 8-12 April 2014
University College London, CA, 28-29 April 2014
Milan, Italy, CA, 5-9 July 2014
Kelly A. Langert, Cynthia L. Von Zee and Evan B. Stubbs
Recruitment and trafficking of autoreactive leucocytes across the blood-nerve barrier is an early pathological insult in Guillain-Barré syndrome. Although the aetiology and pathogenesis of this syndrome remains unclear, pro-inflammatory cytokines, such as TNFα, are reported to be elevated in the early course of the disease, and may initiate nerve injury by activating the blood-nerve barrier. The paper by Langert et al. shows that in peripheral nerve microvascular endoneurial endothelial cells TNFα causes dose- and time-dependent increases in CCL2 and ICAM-1 content, potentially facilitating recrutiment and trafficking of autoreactive leucocytes across the blood-nerve barrier in autoimmune disorders such as Gullain-Barré syndrome.
Juan Xiong, Maria Burkovetskaya, Nikolay Karpuk and Tammy Kielian
Staphylococcus aureus is a common aetiological agent of bacterial brain abscesses. We have previously established that a considerable IL-1 (interleukin-1) response is elicited immediately following S. aureus infection, where the cytokine can exert pleiotropic effects on glial activation and blood-brain barrier permeability. The results of the present study by Kielian and colleagues demonstrate that IL-1RI signalling plays a pivotal role in the genesis of immune responses during the acute stage of brain abscess development through S. aureus containment, inflammatory mediator production, peripheral immune cell recruitment, and regulation of astrocyte hemichannel activity, advancing understanding of MyD88-dependent cascades and implicating IL-1RI signalling as a major antimicrobial effector pathway during acute brain-abscess formation.
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