Christopher S. Colwell
Los Angeles, U.S.A.
Scott T. Brady
Chicago, U.S.A.Wilma J. Friedman
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, JapanWendy 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.
Anthony T. Campagnoni
Los Angeles, U.S.A.
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.
Yossan‑Var Tan and James A Waschek
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
Tumour necrosis factor α enhances CCL2 and ICAM-1 expression in peripheral nerve microvascular endoneurial endothelial cells
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.
IL-1RI (interleukin-1 receptor type I) signalling is essential for host defence and hemichannel activity during acute central nervous system bacterial infection
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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