Combined nasal administration of encephalitogenic myelin basic protein peptide 68-86 and IL-10 suppressed incipient experimental allergic encephalomyelitis in Lewis rats.

Important note: Information in this article was accurate in 2000. The state of the art may have changed since the publication date.

Combined nasal administration of encephalitogenic myelin basic protein peptide 68-86 and IL-10 suppressed incipient experimental allergic encephalomyelitis in Lewis rats.

Clin Immunol. 2000 Sep;96(3):205-11. Unique Identifier : AIDSLINE MED/20423208
Xu LY; Yang JS; Huang YM; Levi M; Link H; Xiao BG; Experimental Neurobiology Unit and Neuroimmunology Unit,; Karolinska Institute, Stockholm, Sweden.

Abstract: Mucosal administration of low doses of myelin basic protein (MBP) peptide 68-86 (MBP 68-86) or anti-inflammatory cytokine IL-10 effectively prevented experimental allergic encephalomyelitis (EAE), but failed to suppress the disease if given after 7 days postimmunization (p.i.), i.e., after T cell priming had occurred. We anticipated that combined administration of autoantigen and IL-10 can treat incipient EAE. Lewis rats with EAE actively induced with MBP 68-86 and complete Freund's adjuvant received 120 &mgr;g MBP 68-86 + 200 ng IL-10 per rat per day from day 7 p.i. and for 5 consecutive days. These rats showed later onset, lower clinical scores, less body weight loss, and shorter duration of EAE than rats receiving MBP 68-86 or IL-10 only or PBS. EAE amelioration was associated with decreased infiltration of ED1(+) macrophages and CD4(+) T cells within the central nervous system and with decreased proliferative responses of lymph node cells, indicating that combined administration of MBP 68-86 and IL-10 induced immune hyporesponsiveness. IFN-gamma secretion as well as IFN-gamma, TNF-alpha, IL-4, and IL-10 mRNA expression by lymph node MNC was down-regulated in the treated rats. Immune hyporesponsiveness, rather than immune deviation or regulatory mechanisms, seems to be responsible for the protection of EAE after autoantigen + IL-10 administration by the nasal route. Copyright 2000 Academic Press.

Keywords: JOURNAL ARTICLE Administration, Intranasal Administration, Oral Animal Antigens/PHARMACOLOGY Cytokines/GENETICS Drug Therapy, Combination Encephalomyelitis, Experimental Autoimmune/*DRUG THERAPY/ IMMUNOLOGY/PREVENTION & CONTROL Immune Tolerance/DRUG EFFECTS Immunohistochemistry Interferon Type II/SECRETION Interleukin-10/*ADMINISTRATION & DOSAGE/*THERAPEUTIC USE Lymph Nodes/CYTOLOGY Lymphocyte Transformation/DRUG EFFECTS Monocytes/CHEMISTRY Myelin Basic Proteins/*ADMINISTRATION & DOSAGE/*THERAPEUTIC USE Peptide Fragments/*ADMINISTRATION & DOSAGE/*THERAPEUTIC USE Rats Rats, Inbred Lew RNA, Messenger/METABOLISM Support, Non-U.S. Gov't Th1 Cells/SECRETION

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