Neuroimmune Pharmacological Control of EAE

Pahan, Kalipada

doi:10.1007/s11481-010-9219-6

Cited by 30 publications

(40 citation statements)

References 11 publications

(11 reference statements)

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“…2 is the most common human demyelinating disorder of the CNS in which promoting remyelination remains a crucial therapeutic challenge (1)(2)(3)(4). Although neurotrophins (nerve growth factor, neurotrophin-3 (NT-3), NT-4/5, and brain-derived neurotrophic factor) and glial cell line-derived neurotrophic factor-related factors (glial cell linederived neurotrophic factor and neurturin) do not increase myelinogenesis, ciliary neurotrophic factor (CNTF) induces a strong promyelinating effect (5).…”

Section: Multiple Sclerosis (Ms)mentioning

confidence: 99%

Up-regulation of Ciliary Neurotrophic Factor in Astrocytes by Aspirin

Modi

Sendtner

Pahan

2013

Journal of Biological Chemistry

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Section: Multiple Sclerosis (Ms)mentioning

confidence: 99%

Up-regulation of Ciliary Neurotrophic Factor in Astrocytes by Aspirin

Modi

Sendtner

Pahan

2013

Journal of Biological Chemistry

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“…For the purposes of this research, different models of experimental demyelination were used under experimental conditions (Baxter, 2007;Pahan, 2010). people worldwide aged 18 or more years, the peak of contracting it being between 25 and 35 years of age (Coote et al, 2013).…”

Section: Inflammation and The Central Nervous System (Cns) Inflammatimentioning

confidence: 99%

Neuroinflammation and demyelination from the point of nitrosative stress as a new target for neuroprotection

Ljubisavljević¹,

Stojanović²

2015

Reviews in the Neurosciences

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AbstractThe role of nitrosative stress in the early pathogenesis of neuroinflammation and demyelination is undoubtedly wide. This review summarizes and integrates the results, found in previously performed studies, which have evaluated nitrosative stress participation in neuroinflammation. The largest number of studies indicates that the supply of nitrosative stress inhibitors has led to the opposite clinical effects in experimental studies. Some results claim that attributing the protective role to nitric oxide, outside the total changes of redox oxidative processes and without following the clinical and paraclinical correlates of neuroinflammation, is an overrated role of this mediator. The fact is that the use of nitrosative stress inhibitors would be justified in the earlier phases of neuroinflammation. The ideal choice would be a specific inducible nitric oxide synthase (iNOS) inhibitor, because its use would preserve the physiological features of nitric oxide produced by the effects of constitutive NOS. This review discusses the antinitrosative therapy as a potential mode of therapy that aims to control neuroinflammation in early phases, delaying its later phases, which are accompanied with irreversible neurological disabilities. Some parameters of nitrosative stress might serve as surrogate biomarkers for neuroinflammation intensity and its radiological and clinical correlates.

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“…T cells play a key role in immunostimulation and immunoregulation [1–3]. Upon activation by various physiological and pathophysiological cues, CD4 + T cells can differentiate into different lineages of T helper (Th) cells with distinct biological functions (Figure 1).…”

mentioning

confidence: 99%

“…On the other hand, transcription factors like GATA- 3 and STAT6 drive the generation of Th2 cells that produce ant-iinflammatory cytokines (IL-4, IL-10 and IL-13) and mediate humoral immunity. It is known that autoimmune diseases are mainly mediated by Th1 response and that switching of Th1 to a Th2 phenotype is a way to ameliorate autoimmune diseases [3–6]. However, this hypothesis is being challenged as after the discovery of IL-23, one new T helper cell (Th17) has been identified (Figure 1) that expresses signature transcription factor RORγT and secretes IL-17 and IL-21 [7].…”

mentioning

confidence: 99%

“…However, this hypothesis is being challenged as after the discovery of IL-23, one new T helper cell (Th17) has been identified (Figure 1) that expresses signature transcription factor RORγT and secretes IL-17 and IL-21 [7]. Although Th17 cells are involved in the host defense against bacteria, fungi, and viruses, these cells are nowadays considered to play a more active role than Th1 cells in the disease process of multiple sclerosis (MS) and other autoimmune disorders [2,3,7]. …”

mentioning

confidence: 99%

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