Combined Treatment of Acute EAE in Lewis Rats with TNF-Binding Protein and Interleukin-1 Receptor Antagonist

Wiemann, B; Van, Gwenneth; Danilenko, Dimitry M.; Qiao, Yan; Matheson, Christine R.; Munyakazi, L.; Ogenstad, Stephan; Starnes, C.O.

doi:10.1006/exnr.1997.6723

Cited by 24 publications

(13 citation statements)

References 50 publications

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“…In addition, proinflammatory cytokines such as TNFα and IL-6 are also considered important for induction and pathogenesis involving inflammation and neuroglial damage (Penkowa and Hidalgo, 2001; Villarroya et al, 1997; Wiemann et al, 1998). To study the cytokine production, splenocytes from MOG-immunized mice after CS-A or CSPG-DS treatment were washed, fixed and permeabilized.…”

Section: Resultsmentioning

confidence: 99%

“…Proinflammatory cytokines such as TNFα and IL-6 are considered important for induction and pathogenesis of EAE/MS disease, which is characterized by significant inflammation and neuroglial damage (Penkowa and Hidalgo, 2001; Villarroya et al, 1997; Wiemann et al, 1998). It has also been reported that CSPG-DS markedly alleviated the clinical symptoms of EAE and protected against the neuronal loss in EAU (Rolls et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

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Immune modulation by chondroitin sulfate and its degraded disaccharide product in the development of an experimental model of multiple sclerosis

Zhou

Nagarkatti

Yin

et al. 2010

Journal of Neuroimmunology

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Clinical symptoms in MOG-induced EAE mice significantly exacerbated following hondroitin sulfate A (CS-A) injection, whereas administration of a degraded product, CSPG-DS, caused dramatic inhibition of EAE development. Also, administration of CSPG-DS but not CS-A, after the onset of clinical symptoms of EAE, was able to suppress the disease. Further studies demonstrated that CS-A up-regulated STAT4 expression and thus, induced IFN-γ production and Th1 CD4 T cell differenttiation. CS-A also up-regulated STAT3 and IL-23 expression and thus increased IL-17 producing T cells. CSPG-DS treatment both in vivo and in vitro decreased TNFα production from splenocytes. In vitro and in vivo studies indicated that CSPG-DS treatment in EAE mice significantly blocked migration of lymphocytes, whereas CS-A treatment increased lymphocyte infiltration in the brain.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Immune modulation by chondroitin sulfate and its degraded disaccharide product in the development of an experimental model of multiple sclerosis

Zhou

Nagarkatti

Yin

et al. 2010

Journal of Neuroimmunology

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“…Six cytokines were tested as potential candidates, including IL1-RA, IL-2, IL-4, IL-10, IL-13, and IL-16. IL-1RA and IL-16 were predicted to have pronounced antiinflammatory activity (11)(12)(13)(14)(15). IL-4 and IL-13 were predicted to drive immune deviation toward a nonpathogenic Th2 lineage (16,17).…”

Section: Discussionmentioning

confidence: 99%

A Fusion Protein Consisting of IL-16 and the Encephalitogenic Peptide of Myelin Basic Protein Constitutes an Antigen-Specific Tolerogenic Vaccine That Inhibits Experimental Autoimmune Encephalomyelitis

Mannie

Abbott

2007

The Journal of Immunology

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To test a novel concept for the generation of tolerogenic vaccines, fusion proteins were constructed encompassing a tolerogenic or biasing cytokine and the major encephalitogenic peptide of guinea pig myelin basic protein (GPMBP; i.e., neuroantigen or NAg). The cytokine domain was predicted to condition APC while simultaneously targeting the covalently linked encephalitogenic peptide to the MHC class II Ag processing pathway of those conditioned APC. Rats were given three s.c. injections of cytokine-NAg in saline 1–2 wk apart and then at least 1 wk later were challenged with NAg in CFA. The rank order of tolerogenic activity in the Lewis rat model of EAE was NAgIL16 > IL2NAg > IL1RA-NAg, IL13NAg ≥ IL10NAg, GPMBP, GP69–88, and saline. NAgIL16 was also an effective inhibitor of experimental autoimmune encephalomyelitis when administered after an encephalitogenic challenge during the onset of clinical signs. Covalent linkage of the NAg and IL-16 was required for inhibition of experimental autoimmune encephalomyelitis. These data identify IL-16 as an optimal cytokine partner for the generation of tolerogenic vaccines and indicate that such vaccines may serve as Ag-specific tolerogens for the treatment of autoimmune disease.

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“…For example, anti-TNF␣ antibodies as well as soluble TNF receptors prevents the development of EAE in rodents immunized with MBP. Treatment of rats during the induction phase of EAE with IL-1ra protected these animals from EAE (27)(28)(29), and treatment of rats with IL-1ra who received lymph node cells from MBP primed rats also resulted in the development of milder disease. Furthermore, treatment of rats with an IL-1ra during the effector phase of the process resulted in a significant inhibition of clinical signs of EAE (28).…”

mentioning

confidence: 93%

The Induction of EAE Is Only Partially Dependent on TNF Receptor Signaling but Requires the IL-1 Type I Receptor

Schiffenbauer

Streit

Butfiloski

et al. 2000

Clinical Immunology

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Combined Treatment of Acute EAE in Lewis Rats with TNF-Binding Protein and Interleukin-1 Receptor Antagonist

Cited by 24 publications

References 50 publications

Immune modulation by chondroitin sulfate and its degraded disaccharide product in the development of an experimental model of multiple sclerosis

Immune modulation by chondroitin sulfate and its degraded disaccharide product in the development of an experimental model of multiple sclerosis

A Fusion Protein Consisting of IL-16 and the Encephalitogenic Peptide of Myelin Basic Protein Constitutes an Antigen-Specific Tolerogenic Vaccine That Inhibits Experimental Autoimmune Encephalomyelitis

The Induction of EAE Is Only Partially Dependent on TNF Receptor Signaling but Requires the IL-1 Type I Receptor

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