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Mechanisms of suppression of experimental autoimmune encephalomyelitis by intravenous administration of myelin basic protein: role of regulatory spleen cells.
Exp Mol Pathol. 2000 Feb; 68(1):29-37.EM

Abstract

Experimental allergic encephalomyelitis (EAE) can be downregulated by intravenous (iv) administration of myelin basic protein (MBP). In this report we show that downregulation of EAE by two 500-microgram doses of MBP administered iv before immunization was associated with reduced encephalitogenicity of both spleen and lymph node cells (day 12 postimmunization) in adoptive transfer studies. However, efficient downregulation of EAE by two 500-microgram iv doses of MBP on days 10 and 11 after active immunization (at the time of disease onset) was associated with no significant change in the encephalitogenicity of lymph node cells, but a complete abrogation of the ability of spleen cells (both at day 12 postimmunization) to transfer EAE compared to controls. Furthermore, coculture of spleen cells from rats tolerized by iv MBP on days 10 and 11 after active immunization with MBP with MBP-reactive T cells resulted in a decreased ability of the spleen T cells to transfer EAE compared to effector cells in monoculture. In contrast, coculture of MBP-reactive T cells with spleen cells from rats tolerized by iv MBP on days 14 and 7 before active immunization resulted in increased disease in recipient rats. These results suggest that reversal of clinical EAE by iv injection of MBP at the time of disease onset is due at least in part to a T cell control mechanism located in the spleen and suggest the presence of splenocyte regulatory cells that can suppress the ability of encephalitogenic T cells to induce EAE.

Authors+Show Affiliations

Department of Neurology, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, Pennsylvania, 19104-4283, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10640452

Citation

Hilliard, B A., et al. "Mechanisms of Suppression of Experimental Autoimmune Encephalomyelitis By Intravenous Administration of Myelin Basic Protein: Role of Regulatory Spleen Cells." Experimental and Molecular Pathology, vol. 68, no. 1, 2000, pp. 29-37.
Hilliard BA, Kamoun M, Ventura E, et al. Mechanisms of suppression of experimental autoimmune encephalomyelitis by intravenous administration of myelin basic protein: role of regulatory spleen cells. Exp Mol Pathol. 2000;68(1):29-37.
Hilliard, B. A., Kamoun, M., Ventura, E., & Rostami, A. (2000). Mechanisms of suppression of experimental autoimmune encephalomyelitis by intravenous administration of myelin basic protein: role of regulatory spleen cells. Experimental and Molecular Pathology, 68(1), 29-37.
Hilliard BA, et al. Mechanisms of Suppression of Experimental Autoimmune Encephalomyelitis By Intravenous Administration of Myelin Basic Protein: Role of Regulatory Spleen Cells. Exp Mol Pathol. 2000;68(1):29-37. PubMed PMID: 10640452.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanisms of suppression of experimental autoimmune encephalomyelitis by intravenous administration of myelin basic protein: role of regulatory spleen cells. AU - Hilliard,B A, AU - Kamoun,M, AU - Ventura,E, AU - Rostami,A, PY - 2000/1/21/pubmed PY - 2000/3/4/medline PY - 2000/1/21/entrez SP - 29 EP - 37 JF - Experimental and molecular pathology JO - Exp Mol Pathol VL - 68 IS - 1 N2 - Experimental allergic encephalomyelitis (EAE) can be downregulated by intravenous (iv) administration of myelin basic protein (MBP). In this report we show that downregulation of EAE by two 500-microgram doses of MBP administered iv before immunization was associated with reduced encephalitogenicity of both spleen and lymph node cells (day 12 postimmunization) in adoptive transfer studies. However, efficient downregulation of EAE by two 500-microgram iv doses of MBP on days 10 and 11 after active immunization (at the time of disease onset) was associated with no significant change in the encephalitogenicity of lymph node cells, but a complete abrogation of the ability of spleen cells (both at day 12 postimmunization) to transfer EAE compared to controls. Furthermore, coculture of spleen cells from rats tolerized by iv MBP on days 10 and 11 after active immunization with MBP with MBP-reactive T cells resulted in a decreased ability of the spleen T cells to transfer EAE compared to effector cells in monoculture. In contrast, coculture of MBP-reactive T cells with spleen cells from rats tolerized by iv MBP on days 14 and 7 before active immunization resulted in increased disease in recipient rats. These results suggest that reversal of clinical EAE by iv injection of MBP at the time of disease onset is due at least in part to a T cell control mechanism located in the spleen and suggest the presence of splenocyte regulatory cells that can suppress the ability of encephalitogenic T cells to induce EAE. SN - 0014-4800 UR - https://www.unboundmedicine.com/medline/citation/10640452/Mechanisms_of_suppression_of_experimental_autoimmune_encephalomyelitis_by_intravenous_administration_of_myelin_basic_protein:_role_of_regulatory_spleen_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4800(99)92290-6 DB - PRIME DP - Unbound Medicine ER -