CD4+ T cells from Copolymer-1 immunized mice protect dopaminergic neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease

Laurie, C Doering; Reynolds, Ashley D.; Coskun, Ozlem; Bowman, Erik; Gendelman, Howard E.; Mosley, R. Lee

doi:10.1016/j.jneuroim.2006.11.009

Cited by 91 publications

(64 citation statements)

References 30 publications

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“…Moreover, this protection occurred in a dose-dependent manner (Laurie et al 2007). There is some evidence that copolymer-1 is a potent inducer of regulatory T cells (Treg) (Arnon and Aharoni 2004), and it is possible that a specific subset of CD4+ T cells were activated by copolymer-1 and mediated the main protective effect.…”

Section: Peripheral T Lymphocytes Are Involved In the Progression Of Pdmentioning

confidence: 96%

“…In PD patients, persistent activation of microglia has been observed (Gerhard et al 2006). Activated microglia have also been found in the SN and/or striatum in animal models of PD (Czlonkowska et al 1996;Kohutnicka et al 1998;Laurie et al 2007;Kim et al 2009). An accumulation of activated microglia around dopaminergic neurons has been found in three post-mortem human brains with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism (Langston et al 1999).…”

Section: Functional States Of Microglia In Pdmentioning

confidence: 99%

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Activated Immune Cells in Parkinson's Disease

Cao

Shen

2011

J Neuroimmune Pharmacol

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Recently, an interaction between neurodegenerative processes and the innate and adaptive immune responses has been increasingly recognized. Activation of microglia, infiltration of peripheral T lymphocytes, and T-cell interaction with microglia may strongly affect the progression of Parkinson's disease (PD) both in patients and in animal models of the disease. Here, we summarize the current knowledge regarding the role of microglia in the progression of PD. The plasticity of the microglial response is also discussed in the context of PD. In addition, we also focus on the influence of several peripheral T-cell subsets on PD progression as well as on possible pathways by which they might act. This review should help increase our understanding of the effects of innate and adaptive immune cells in the pathogenesis of PD.

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Section: Peripheral T Lymphocytes Are Involved In the Progression Of Pdmentioning

confidence: 96%

Section: Functional States Of Microglia In Pdmentioning

confidence: 99%

Activated Immune Cells in Parkinson's Disease

Cao

Shen

2011

J Neuroimmune Pharmacol

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“…On the other hand, Gendelman and colleagues demonstrated that T cells from mice immunized with Copolymer-1 (Cop-1), are able to attenuate microglial responses and lead to neuroprotection in a MPTP mouse model of PD (Benner et al, 2004). This neuroprotective effect was later found to be mediated by the CD4 + type of T cells, suggesting the possible involvement of Treg cells (Laurie et al, 2007). Later work by the same group confirmed this hypothesis by showing that passive transfer to MPTP mice of activated Treg cells, but not effector T cells, efficiently suppressed microglial activation and afforded neuroprotection (Reynolds et al, 2007), suggesting that the immunomodulating abilities of Treg cells could potentially be utilized as a therapeutic approach against PD (Stone et al, 2009).…”

Section: Prospects For Syn-based Immunotherapy In Pdmentioning

confidence: 99%

Alpha-Synuclein and the Immune Response in Parkinson’s Disease

Roodveldt¹,

Labrador-Garrido²,

Izquierdo³

et al. 2011

Towards New Therapies for Parkinson's Disease

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“…Anti-inflammatory action can occur at many different sites along any inflammatory cascade. It is therefore logical that anti-inflammatory medications such as non-steroidal anti-inflammatory drugs, anti-cytokines, immunosuppressants such as tacrolimus and immunomodulators such as copolymer-1 that reduce inflammation may be formally tested in pre-clinical and clinical trials, alone or as adjuvants to other therapeutic interventions (Laurie et al 2007;Smith et al 2009;Sobrado et al 2009;Tansey and Goldberg 2009).…”

Section: Anti-inflammatory Therapymentioning

confidence: 99%

Therapeutic approaches for neuronopathic lysosomal storage disorders

Schiffmann

2010

J of Inher Metab Disea

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Therapy of the central nervous system (CNS) manifestations of lysosomal storage diseases (LSDs) has remained a major challenge because of its inability to deliver therapeutic agents efficiently across the intact blood-brain barrier. Non-specific therapies such as hematopoietic stem cell transplantation have been useful in globoid cell leukodystrophy (Krabbe disease) and in some mucopolysaccharidoses. Anti-inflammatory agents also show promise as adjuvant therapy. High doses of replacement therapy with native or modified enzyme show renewed promise for correction of CNS cells. Alternatively, small molecules can enter the brain relatively easily and promote reduction of accumulated substrate or function as pharmacological chaperones to enhance the level of the deficient enzyme. Gene therapy is still being developed and tested in patients. It is therefore likely that, thanks to a better understanding of disease mechanism, a variety of therapeutic approaches, used alone or in combination, will be useful to treat the devastating neurological complications of LSDs.

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CD4+ T cells from Copolymer-1 immunized mice protect dopaminergic neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease

Cited by 91 publications

References 30 publications

Activated Immune Cells in Parkinson's Disease

Activated Immune Cells in Parkinson's Disease

Alpha-Synuclein and the Immune Response in Parkinson’s Disease

Therapeutic approaches for neuronopathic lysosomal storage disorders

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