Chi Wang Ip

Role of immune cells in animal models for inherited peripheral neuropathies.

Immune cells contribute to myelin degeneration and axonopathic changes in mice overexpressing proteolipid protein in oligodendrocytes.

Polyclonal expansion of regulatory T cells interferes with effector cell migration in a model of multiple sclerosis.

Sialoadhesin deficiency ameliorates myelin degeneration and axonopathic changes in the CNS of PLP overexpressing mice.

Antigen therapy of experimental autoimmune encephalomyelitis selectively induces apoptosis of pathogenic T cells.

Monocyte chemoattractant protein-1 is a pathogenic component in a model for a hereditary peripheral neuropathy.

Origin of CD11b+ macrophage-like cells in the CNS of PLP-overexpressing mice: low influx of haematogenous macrophages and unchanged blood-brain-barrier in the optic nerve.

Increased number of microglia in the brain of severe combined immunodeficient (SCID) mice.

Transient widespread blood-brain barrier alterations after cerebral photothrombosis as revealed by gadofluorine M-enhanced magnetic resonance imaging.

The co-inhibitory molecule PD-1 modulates disease severity in a model for an inherited, demyelinating neuropathy.

Tacrolimus (FK506) causes disease aggravation in models for inherited peripheral myelinopathies.

PD-1 regulates neural damage in oligodendroglia-induced inflammation.

Accelerated course of experimental autoimmune encephalomyelitis in PD-1-deficient central nervous system myelin mutants.

Collateral neuronal apoptosis in CNS gray matter during an oligodendrocyte-directed CD8(+) T cell attack.

Ectopic T-cell specificity and absence of perforin and granzyme B alleviate neural damage in oligodendrocyte mutant mice.

Neuroinflammation by cytotoxic T-lymphocytes impairs retrograde axonal transport in an oligodendrocyte mutant mouse.

Immune cells perturb axons and impair neuronal survival in a mouse model of infantile neuronal ceroid lipofuscinosis.

CD8⁺ T cell help is required for efficient induction of EAE in Lewis rats.

Lymphocytes reduce nigrostriatal deficits in the 6-hydroxydopamine mouse model of Parkinson's disease.

Tor1a+/- mice develop dystonia-like movements via a striatal dopaminergic dysregulation triggered by peripheral nerve injury.

AAV1/2-induced overexpression of A53T-α-synuclein in the substantia nigra results in degeneration of the nigrostriatal system with Lewy-like pathology and motor impairment: a new mouse model for Parkinson's disease.

Pathogenic inflammation in the CNS of mice carrying human PLP1 mutations.

Subthalamic nucleus deep brain stimulation is neuroprotective in the A53T α-synuclein Parkinson's disease rat model.

Reply to "Can STN DBS protect both nigral somata and innervation of the striatum?"

Generation and Analysis of Viral Vector-Mediated Rodent Models for Parkinson's Disease.

Striatal dopaminergic dysregulation and dystonia-like movements induced by sensorimotor stress in a pharmacological mouse model of rapid-onset dystonia-parkinsonism.

The evolution of dystonia-like movements in TOR1A rats after transient nerve injury is accompanied by dopaminergic dysregulation and abnormal oscillatory activity of a central motor network.