Tags

Type your tag names separated by a space and hit enter

The complexicity of cytokine treatment in ongoing EAE induced with MBP peptide 68-86 in Lewis rats.
Clin Immunol. 2000 Apr; 95(1 Pt 1):70-8.CI

Abstract

IL-10 and TGF-beta1 are important immunoregulatory cytokines associated with clinical remissions in multiple sclerosis and amelioration of experimental allergic encephalomyelitis (EAE). IL-10 and TGF-beta1 have previously been shown to prevent the development of EAE. Here, we study effects of IL-10 and TGF-beta1 in ongoing EAE. When IL-10 or TGF-beta1 was administered by the nasal route from day 0 to day 7 postimmunization (pi), both IL-10 and TGF-beta1 prevented the development of acute EAE in Lewis rats. When IL-10 or TGF-beta1 was administered by the nasal route from day 5 to day 12 pi, both IL-10 and TGF-beta1 failed to influence clinical EAE. The inhibition of clinical EAE severity in IL-10-prevented rats was associated with reduced proliferation, IFN-gamma mRNA expression, and IFN-gamma secretion, while proliferation as well as IFN-gamma mRNA expression and secretion were augmented in TGF-beta1-prevented rats. TGF-beta1-prevented rats exhibited high levels of NO production by DC, which may mediate apoptosis of CD4+ T cells and of the DC themselves. For prevention, both IL-10 and TGF-beta1 inhibited infiltration of CD4+ T cells within the CNS, but neither IL-10 nor TGF-beta1 induced immune deviation from Th1 to Th2. Expression of IL-4 mRNA was not altered in IL-10- and TGF-beta1-prevented rats. These results demonstrate that IL-10 and TGF-beta administration by the nasal route can prevent the development of acute EAE, but by different mechanisms. The findings in rats with ongoing EAE have implications for the clinical application of cytokine treatment in autoimmune diseases.

Authors+Show Affiliations

Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10794434

Citation

Xu, L Y., et al. "The Complexicity of Cytokine Treatment in Ongoing EAE Induced With MBP Peptide 68-86 in Lewis Rats." Clinical Immunology (Orlando, Fla.), vol. 95, no. 1 Pt 1, 2000, pp. 70-8.
Xu LY, Ishikawa M, Huang YM, et al. The complexicity of cytokine treatment in ongoing EAE induced with MBP peptide 68-86 in Lewis rats. Clin Immunol. 2000;95(1 Pt 1):70-8.
Xu, L. Y., Ishikawa, M., Huang, Y. M., Levi, M., van der Meide, P. H., Wahren, B., Link, H., & Xiao, B. G. (2000). The complexicity of cytokine treatment in ongoing EAE induced with MBP peptide 68-86 in Lewis rats. Clinical Immunology (Orlando, Fla.), 95(1 Pt 1), 70-8.
Xu LY, et al. The Complexicity of Cytokine Treatment in Ongoing EAE Induced With MBP Peptide 68-86 in Lewis Rats. Clin Immunol. 2000;95(1 Pt 1):70-8. PubMed PMID: 10794434.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The complexicity of cytokine treatment in ongoing EAE induced with MBP peptide 68-86 in Lewis rats. AU - Xu,L Y, AU - Ishikawa,M, AU - Huang,Y M, AU - Levi,M, AU - van der Meide,P H, AU - Wahren,B, AU - Link,H, AU - Xiao,B G, PY - 2000/5/4/pubmed PY - 2000/5/20/medline PY - 2000/5/4/entrez SP - 70 EP - 8 JF - Clinical immunology (Orlando, Fla.) JO - Clin. Immunol. VL - 95 IS - 1 Pt 1 N2 - IL-10 and TGF-beta1 are important immunoregulatory cytokines associated with clinical remissions in multiple sclerosis and amelioration of experimental allergic encephalomyelitis (EAE). IL-10 and TGF-beta1 have previously been shown to prevent the development of EAE. Here, we study effects of IL-10 and TGF-beta1 in ongoing EAE. When IL-10 or TGF-beta1 was administered by the nasal route from day 0 to day 7 postimmunization (pi), both IL-10 and TGF-beta1 prevented the development of acute EAE in Lewis rats. When IL-10 or TGF-beta1 was administered by the nasal route from day 5 to day 12 pi, both IL-10 and TGF-beta1 failed to influence clinical EAE. The inhibition of clinical EAE severity in IL-10-prevented rats was associated with reduced proliferation, IFN-gamma mRNA expression, and IFN-gamma secretion, while proliferation as well as IFN-gamma mRNA expression and secretion were augmented in TGF-beta1-prevented rats. TGF-beta1-prevented rats exhibited high levels of NO production by DC, which may mediate apoptosis of CD4+ T cells and of the DC themselves. For prevention, both IL-10 and TGF-beta1 inhibited infiltration of CD4+ T cells within the CNS, but neither IL-10 nor TGF-beta1 induced immune deviation from Th1 to Th2. Expression of IL-4 mRNA was not altered in IL-10- and TGF-beta1-prevented rats. These results demonstrate that IL-10 and TGF-beta administration by the nasal route can prevent the development of acute EAE, but by different mechanisms. The findings in rats with ongoing EAE have implications for the clinical application of cytokine treatment in autoimmune diseases. SN - 1521-6616 UR - https://www.unboundmedicine.com/medline/citation/10794434/The_complexicity_of_cytokine_treatment_in_ongoing_EAE_induced_with_MBP_peptide_68_86_in_Lewis_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1521661600948332 DB - PRIME DP - Unbound Medicine ER -