Interleukin-1 in the Cerebrospinal Fluid in Chronic Relapsing Experimental Allergic Encephalomyelitis

Symons, J. A.; Bundick, R. V.; Suckling, A.J.; Rumsby, Martin G.

doi:10.1007/978-1-4899-5348-3_44

Cited by 11 publications

(15 citation statements)

References 11 publications

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“…Furthermore, after fractionation we obtained lower activity than in unfractionated serum. A finding in close agreement with this hypothesis is reported in a study [27] in which an increase in plasma IL-1 like activity in the acute phase of chronic relapsing experimental allergic encephalomyelitis (CR-EAE) (one of the experimental models for MS) and a constant increase in CSF IL-1 like activity in the post-acute phase were demonstrated. No statistically significant difference was in fact found between MS patients and normal control serum, nor among the different MS groups.…”

Section: Discussionsupporting

confidence: 85%

“…Column fractionation [6] or filtration and dialysis [27] are believed to be necessary in order to isolate these two lymphokines, as they permit the removal ofaU possible inhibitors. Column fractionation [6] or filtration and dialysis [27] are believed to be necessary in order to isolate these two lymphokines, as they permit the removal ofaU possible inhibitors.…”

Section: Discussionmentioning

confidence: 99%

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Lymphocyte activating factor activity in the serum and cerebrospinal fluid of patients with multiple sclerosis

et al. 1990

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Serum and cerebrospinal fluid (CSF) from patients with multiple sclerosis (MS), patients with other (non-inflammatory) neurological diseases (OND), patients with non-inflammatory non-neurological diseases, and normal controls were assayed for lymphocyte activating factor (LAF) activity by thymocyte costimulation. LAF activity was detected in normal control sera, which did not differ significantly in this respect from MS or OND patient sera. Not were there significant differences by stage of MS (chronic progressive MS, MS in relapse and MS in remission) or between MS patients and the non-inflammatory non-neurological controls. Almost all the CFSs assayed presented lower values than did the corresponding sera. Serum and CSF after fractionation showed no significant increase in LAF activity except in the 2 MS patients in remission. From these data it may be assumed that LAF activity does not necessarily correspond to the clinical phase of MS. The possible role of LAF activity as a marker of MS progression has yet to be determined.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Lymphocyte activating factor activity in the serum and cerebrospinal fluid of patients with multiple sclerosis

et al. 1990

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“…IL-1b is involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and multiple sclero- [21]. It is suggested to act as a mediator in neuronal apoptosis in vitro and in vivo, IL-1b mRNA has been found in MS plaques and in CSF of the EAE mice [22].…”

Section: Discussionmentioning

confidence: 99%

MPTP-induced central dopamine depletion exacerbates experimental autoimmune encephalomyelitis (EAE) in C57BL mice

Bałkowiec-Iskra

Kurkowska‐Jastrzębska

Joniec

et al. 2007

Inflamm. res.

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It is obvious that the central nervous system plays a role in the regulation of an immune response. However, the mechanisms of this regulation are poorly understood. The goal of the present study was to examine the role of one of the neurotransmitters - dopamine, in this process. We used experimental autoimmune encephalomyelitis (EAE), an autoimmune disease with its effector phase in the CNS, as a model to study the effect of central dopamine depletion on the development of an immune response. Dopamine depletion was achieved by treatment with 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropiridine (MPTP; 40 mg/kg), whereas EAE was elicited by immunization with MOG 35-55 (150 microg) in complete Freund's adjuvant (CFA), supplemented with Mycobacterium tuberculosis. As determined by HPLC, striatal dopamine contents in mice treated with MPTP were significantly lower compared to vehicle-treated controls. Remarkably, striatal depletion of dopamine prior to EAE induction resulted in an earlier onset of the disease and an augmentation of its clinical signs. Moreover, the striatal dopamine-depleted mice demonstrated an increased concentration of IL-1beta and decreased concentration of TGFbeta in the spinal cord, compared to EAE mice. Since MPTP itself does not have any direct effect on immune cells, it strongly suggests that the observed changes in EAE induction and progression after MPTP administration depended on lower dopamine level. Further studies are required to find out the cellular mechanism of the dopamine action.

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“…In 1987, Symons et al found increased levels of IL-1 activity, measured at the time by a mouse thymocyte proliferation assay, in the plasma and cerebrospinal fluid (CSF) of guinea pigs immunized with spinal cord homogenates to induce a chronic relapsing form of EAE (19). In the same year, using a rat model of passive EAE, Mannie et al showed lymph node cells from EAE-induced rats treated with human IL-1β were more encephalitogenic, and suggested that this effect was via the action of IL-1β on T lymphocytes (20).…”

Section: Established Associations Between Il-1 and Autoimmune Neuroinmentioning

confidence: 99%

New Insights into the Role of IL-1β in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis

Lin

Edelson

2017

The Journal of Immunology

118

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Multiple sclerosis, and its animal model experimental autoimmune encephalomyelitis, are neuroinflammatory diseases driven by autoreactive pathogenic TH cells which elicit demyelination and axonal damage. How TH cells acquire pathogenicity and communicate with myeloid cells and cells of the central nervous system remain unclear. IL-1β is recognized to play an important role in EAE and perhaps MS. Clinical EAE is significantly attenuated in IL-1 receptor-deficient and IL-1β-deficient mice, and IL-1β is found in the blood, cerebrospinal fluid, and CNS lesions of MS patients. Here, we will focus on new reports which elucidate the cellular sources of IL-1β and its actions during EAE, in both lymphoid tissues and within the CNS. Several immune cell types serve as critical producers of IL-1β during EAE, with the cytokine inducing responses in hematopoietic and non-hematopoietic cells. These findings from the EAE model should inspire efforts towards investigating the therapeutic potential of IL-1 blockade in MS.

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Interleukin-1 in the Cerebrospinal Fluid in Chronic Relapsing Experimental Allergic Encephalomyelitis

Cited by 11 publications

References 11 publications

Lymphocyte activating factor activity in the serum and cerebrospinal fluid of patients with multiple sclerosis

Lymphocyte activating factor activity in the serum and cerebrospinal fluid of patients with multiple sclerosis

MPTP-induced central dopamine depletion exacerbates experimental autoimmune encephalomyelitis (EAE) in C57BL mice

New Insights into the Role of IL-1β in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis

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