Intravenous immunoglobulin ameliorates experimental autoimmune encephalomyelitis and reduces neuropathological abnormalities when administered prophylactically

Jørgensen, Signe Humle; Jensen, Poul Erik; Laursen, Henning; Sørensen, Per Soelberg

doi:10.1179/016164105x48798

Cited by 19 publications

(17 citation statements)

References 34 publications

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“…Our finding that high-dose IVIg effectively prevented EAE development is in agreement with previous results in mouse and rat EAE models [14], [23], [24], [34], [35]. Similar to these studies, we also observed a profound effect of IVIg in the inhibition of the expansion of Th1 and Th17 cytokine production by myelin-reactive T cells [14].…”

Section: Discussionsupporting

confidence: 93%

Optimal Attenuation of Experimental Autoimmune Encephalomyelitis by Intravenous Immunoglobulin Requires an Intact Interleukin-11 Receptor

et al. 2014

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BackgroundIntravenous immunoglobulin (IVIg) has been used to treat a variety of autoimmune disorders including multiple sclerosis (MS); however its mechanism of action remains elusive. Recent work has shown that interleukin-11 (IL-11) mRNAs are upregulated by IVIg in MS patient T cells. Both IVIg and IL-11 have been shown to ameliorate experimental autoimmune encephalomyelitis (EAE), an animal model of MS. The objective of this study was to determine whether the protective effects of IVIg in EAE occur through an IL-11 and IL-11 receptor (IL-11R)-dependent mechanism.MethodsWe measured IL-11 in the circulation of mice and IL-11 mRNA expression in various organs after IVIg treatment. We then followed with EAE studies to test the efficacy of IVIg in wild-type (WT) mice and in mice deficient for the IL-11 receptor (IL-11Rα−/−). Furthermore, we evaluated myelin-specific Th1 and Th17 responses and assessed spinal cord inflammation and demyelination in WT and IL-11Rα−/− mice, with and without IVIg treatment. We also examined the direct effects of mouse recombinant IL-11 on the production of IL-17 by lymph node mononuclear cells.ResultsIVIg treatment induced a dramatic surge (>1000-fold increase) in the levels of IL-11 in the circulation and a prominent increase of IL-11 mRNA expression in the liver. Furthermore, we found that IL-11Rα−/− mice, unlike WT mice, although initially protected, were resistant to full protection by IVIg during EAE and developed disease with a similar incidence and severity as control-treated IL-11Rα−/− mice, despite initially showing protection. We observed that Th17 cytokine production by myelin-reactive T cells in the draining lymph nodes was unaffected by IVIg in IL-11Rα−/− mice, yet was downregulated in WT mice. Finally, IL-11 was shown to directly inhibit IL-17 production of lymph node cells in culture.ConclusionThese results implicate IL-11 as an important immune effector of IVIg in the prevention of Th17-mediated autoimmune inflammation during EAE.

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Section: Discussionsupporting

confidence: 93%

Optimal Attenuation of Experimental Autoimmune Encephalomyelitis by Intravenous Immunoglobulin Requires an Intact Interleukin-11 Receptor

et al. 2014

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“…19,20 Extended observation observed a trend for the delayed progression of the disease in the IVIG treated patients as seen from the change in the EDSS scores. However, these preliminary results need to be confirmed prospectively in a larger number of patients.…”

Section: Edss Evaluation During the Clinical Coursementioning

confidence: 90%

Neurodegenerative central nervous system disease as late sequelae of Langerhans cell histiocytosis. Report from the Japan LCH Study Group

Imashuku¹,

Shibata²,

Kobayashi³

et al. 2008

Haematologica

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Clinical features, brain magnetic resonance imaging findings and EDSS scores of 11 patients with neurodegenerative central nervous system Langerhans cell histiocytosis were analyzed in Japan. All patients initially had multi-system-type Langerhans cell histiocytosis; 8 at 1-2 years of age and 3 at a later age. Neurodegenerative central nervous system largermans cell histiocytosis disease developed after a median time interval of 3.9 years from initial diagnosis. With a median follow-up of 4.5 years, 6 patients showed progression of disease with an EDSS score >3. This study demonstrates the importance of early detection of neurodegenerative central nervous system Langerhans cell histiocytosis by brain magnetic resonance imaging, particularly in the follow-up of patients who developed multi-system-type Langerhans cell histiocytosis in early infancy.Key words: Langerhans cell histiocytosis, late sequelae, neurodegenerative central nervous system disease Imashuku S, Shioda Y, Kobayashi R, Hosoi G, Fujino H, Seto S, Wakita H, Oka A, Okazaki N, Fujita N, Minato T, Koike K, Tsunematsu Y, Morimoto A, and the Japan LCH Study Group (JLSG). Neurodegenerative central nervous system disease as late sequelae of Langerhans cell histiocytosis. Report from the Japan LCH Study Group. Haematologica 2008; 93(4):615-618.

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“…We induced this type of EAE in the inbred rat strain Dark Agouti (DA) and treated the animals with intravenous infusions of human IVIG (1 g/kg) or a placebo solution after the immunisation procedure [10]. The IVIG infusions were administered at two consecutive days: As prophylactic treatment at the time of EAE induction at days 0 and 1 post immunisation (p.i.…”

Section: Ivig Treatment Of Experimental Autoimmune Encephalomyelitismentioning

confidence: 99%

Intravenous immunoglobulin treatment of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis

Jørgensen

Sørensen

2005

Journal of the Neurological Sciences

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Intravenous immunoglobulin ameliorates experimental autoimmune encephalomyelitis and reduces neuropathological abnormalities when administered prophylactically

Cited by 19 publications

References 34 publications

Optimal Attenuation of Experimental Autoimmune Encephalomyelitis by Intravenous Immunoglobulin Requires an Intact Interleukin-11 Receptor

Optimal Attenuation of Experimental Autoimmune Encephalomyelitis by Intravenous Immunoglobulin Requires an Intact Interleukin-11 Receptor

Neurodegenerative central nervous system disease as late sequelae of Langerhans cell histiocytosis. Report from the Japan LCH Study Group

Intravenous immunoglobulin treatment of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis

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