Browse the latest research summaries in the field of immunology for spinal cord injury patients and caregivers.
Showing 411-420 of 620 results
The Journal of Neuroscience, 2009 • March 25, 2009
This study demonstrates that activated macrophages can simultaneously promote axon regeneration and neurotoxicity in the CNS. Zymosan-activated macrophages (ZAMs) initially enhance axon growth towards...
KEY FINDING: Activated macrophages (ZAMs) increase axon growth towards macrophage foci in the spinal cord, indicating a pro-regenerative effect.
JOURNAL OF NEUROTRAUMA, 2009 • December 1, 2009
This study investigates the efficacy of FTY720, an immunomodulatory drug, in reducing inflammation and promoting functional recovery in a rat model of spinal cord injury (SCI). The hypothesis is that ...
KEY FINDING: FTY720 treatment significantly reduced the infiltration of CD4+ T-helper cells and CD8+ cytotoxic T-cells into the spinal cord lesion site after injury, as shown by flow cytometry.
The Journal of Clinical Investigation, 2009 • October 1, 2009
This study demonstrates that B cells, through antibody production, negatively impact recovery after spinal cord injury (SCI) in mice. Mice lacking B cells exhibit improved locomotor function and reduc...
KEY FINDING: Mice lacking B cells showed improved locomotor recovery and reduced lesion volume compared to wild-type mice after spinal cord injury.
The Journal of Clinical Investigation, 2009 • October 1, 2009
The commentary discusses a study that identifies a new immunopathological mechanism arising after spinal cord injury (SCI) in mice. The study demonstrates that B cells produce pathogenic antibodies th...
KEY FINDING: Spinal cord injury leads to a B cell response that produces pathogenic antibodies.
PNAS, 2009 • December 8, 2009
This study characterizes a system-wide infiltration of macrophages in the PNS of mutant SOD1 mice that accompanies axon degeneration in ventral roots, sciatic nerves, and muscle tissues. The origin an...
KEY FINDING: Macrophages are activated throughout the PNS in mutant SOD1G93A and SOD1G37R transgenic mouse models of ALS.
Brain, 2010 • January 19, 2010
This study characterizes a novel cell preparation method that assesses, quickly and effectively, the changes in the principal immune cell types by flow cytometry in the injured spinal cord, daily for t...
KEY FINDING: The study quantitatively demonstrates a novel time-dependent multiphasic response of cellular inflammation in the spinal cord after spinal cord injury.
J Clin Immunol, 2010 • May 1, 2010
The study identifies natural human IgM antibodies that can promote remyelination in animal models of demyelinating diseases like multiple sclerosis (MS). These antibodies bind to oligodendrocytes and ...
KEY FINDING: Two human IgMs (sHIgM22 and sHIgM46) were identified that promoted significant remyelination in TMEV-infected mice, suggesting potential therapeutic applications.
J Clin Immunol, 2010 • May 1, 2010
Spinal cord injury (SCI) involves a primary mechanical trauma followed by a secondary injury cascade, including neuroinflammation, that exacerbates the initial damage. Neuroinflammation, while importa...
KEY FINDING: IgG can modulate the immune response by inducing apoptosis in leukocytes, neutralizing components of the complement system, and inhibiting the activation of leukocytes.
J Neurosci Res, 2011 • March 1, 2011
The study examines the impact of enhanced neuronal MHCI expression on recovery after spinal cord injury (SCI) using transgenic mice. The results showed that transgenic mice with elevated neuronal MHCI...
KEY FINDING: NSE-Db mice displayed significantly improved locomotor function recovery in all key parameters compared with their locomotor abilities 1 week postlesion.
Journal of Neuroinflammation, 2011 • July 6, 2011
This study investigates whether GSNO promotes neurorepair processes by reducing peroxynitrite levels and oxidative injury in rats after TBI. The results demonstrate that GSNO reduces peroxynitrite, pr...
KEY FINDING: GSNO treatment reduced peroxynitrite, lipid peroxides/aldehydes, BBB leakage, inflammation, and edema in the short term (4-48 hours) following TBI in rats.