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Making Spinal Cord Injury (SCI) Research Accessible to Everyone. Simplified summaries of the latest research, designed for patients, caregivers and anybody who's interested.

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Immunology Research

Browse the latest research summaries in the field of immunology for spinal cord injury patients and caregivers.

Showing 1-10 of 730 results

Spinal Cord InjuryImmunologyNeurology

Transgenic Mice With Enhanced Neuronal Major Histocompatibility Complex Class I Expression Recover Locomotor Function Better After Spinal Cord Injury

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.

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Spinal Cord InjuryRegenerative MedicineImmunology

Acid Fibroblast Growth Factor and Peripheral Nerve Grafts Regulate Th2 Cytokine Expression, Macrophage Activation, Polyamine Synthesis, and Neurotrophin Expression in Transected Rat Spinal Cords

The Journal of Neuroscience, 2011 • March 16, 2011

This study investigates the cellular and molecular changes following peripheral nerve grafts and aFGF treatment that improve hindlimb locomotor function in spinal cord-transected rats. The repair stra...

KEY FINDING: The study found that a combination of peripheral nerve grafts and acidic fibroblast growth factor (aFGF) induced higher levels of interleukin-4 (IL-4), IL-10, and IL-13 in the graft areas of rat spinal cords.

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Regenerative MedicineImmunologyNeurology

Enhancing Central Nervous System Repair-The Challenges

CNS Drugs, 2011 • July 1, 2011

Repair of the central nervous system (CNS) constitutes the integral part in treating neurologic diseases and plays a crucial role in restoring CNS architecture and function. In this review, we discuss...

KEY FINDING: The major challenges of CNS repair include neurodegeneration and pathological obstacles impeding neural cell growth after CNS injury.

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ImmunologyNeurologyBrain Injury

S-Nitrosoglutathione reduces oxidative injury and promotes mechanisms of neurorepair following traumatic brain injury in rats

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.

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ImmunologyNeurologyVeterinary Medicine

Distinct Spatio-Temporal Extracellular Matrix Accumulation within Demyelinated Spinal Cord Lesions in Theiler’s Murine Encephalomyelitis

Brain Pathology, 2012 • January 1, 2012

The study characterized the composition and distribution of spinal cord ECM during TMEV infection to identify underlying molecular mechanisms and transcriptional changes. Microarray analysis revealed ...

KEY FINDING: Progressive accumulation of chondroitin sulfate proteoglycans, glycoproteins, and collagens occurred within demyelinated TME lesions, paralleling astrogliosis development.

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ImmunologyNeurology

CXCR4 Signaling Regulates Remyelination by Endogenous Oligodendrocyte Progenitor Cells in a Viral Model of Demyelination

Glia, 2011 • December 1, 2011

This study investigates the role of CXCR4 signaling in regulating remyelination by endogenous oligodendrocyte progenitor cells (OPCs) in a viral model of demyelination. The findings suggest that CXCR4...

KEY FINDING: CXCR4 signaling is required for OPCs to mature and contribute to remyelination in response to JHMV-induced demyelination.

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ImmunologyNeurology

Wallerian degeneration: Gaining perspective on inflammatory events after peripheral nerve injury

Journal of Neuroinflammation, 2011 • August 30, 2011

Successful peripheral axon regeneration is associated with a rapid and efficient inflammatory response that is terminated in due course. Schwann cells and macrophages communicate via cytokine networks...

KEY FINDING: Axon degeneration in the distal nerve instigates subsequent degenerative processes after PNI; however, axon degeneration does not begin immediately.

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ImmunologyNeurology

Inhibition of soluble tumour necrosis factor is therapeutic in experimental autoimmune encephalomyelitis and promotes axon preservation and remyelination

Brain, 2011 • September 1, 2011

This study investigates the distinct roles of soluble TNF and transmembrane TNF in experimental autoimmune encephalomyelitis (EAE) using pharmacological inhibitors. The researchers found that selectiv...

KEY FINDING: Selective inhibition of soluble TNF with XPro1595 improves the clinical outcome in experimental autoimmune encephalomyelitis (EAE).

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ImmunologyNeurologyBiomedical

Paranodal myelin retraction in relapsing experimental autoimmune encephalomyelitis visualized by coherent anti-Stokes Raman scattering microscopy

Journal of Biomedical Optics, 2011 • October 4, 2011

This study investigates myelin integrity in mice with relapsing experimental autoimmune encephalomyelitis (EAE) using coherent anti-Stokes Raman scattering (CARS) microscopy. The research demonstrates...

KEY FINDING: Paranodal myelin retraction is an early event in relapsing experimental autoimmune encephalomyelitis (EAE), occurring at the onset of the disease and at the borders of acute demyelinating lesions.

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ImmunologyNeurologyGenetics

Reduced inflammation accompanies diminished myelin damage and repair in the NG2 null mouse spinal cord

Journal of Neuroinflammation, 2011 • November 13, 2011

This study examines the role of NG2, a proteoglycan expressed by OPCs, pericytes, and macrophages/microglia, in spinal cord demyelination and remyelination using wild type and NG2 null mice. Results s...

KEY FINDING: The initial volume of spinal cord demyelination in wild type mice is twice as large as in NG2 null mice, suggesting NG2 influences the initial damage phase.

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