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Mechanisms of recovery from experimental allergic encephalomyelitis induced with myelin basic protein peptide 68-86 in Lewis rats: a role for dendritic cells in inducing apoptosis of CD4+ T cells.
J Neuroimmunol. 1999 Jun 01; 97(1-2):25-36.JN

Abstract

Spontaneous remission of experimental allergic encephalomyelitis (EAE) is usually associated with prominent apoptosis. The mechanisms behind apoptosis are unknown. We examined the functions of dendritic cells (DC) from Lewis rats with EAE induced by immunization with myelin basic protein peptide 68-86 (MBP68 - - 86). Recovery from EAE was associated with three major functional changes of freshly prepared DC: (1) elevated proliferation, (2) increased nitric oxide (NO) production, and (3) augmented IFN-gamma secretion. In Freund's complete adjuvant (FCA)-immunized control rats, no increase of proliferation, NO production or IFN-gamma secretion was observed on day 21 post-immunization (p.i.), i.e., recovery from EAE. In vitro effects of IFN-gamma, TNF-alpha, TGF-beta1, IL-4 and IL-10 on DC were examined. IFN-gamma enhanced proliferation and NO production by DC, while TNF-alpha and IL-4 induced only slight DC proliferation. DC from recovering EAE rats (day 21 p.i.) suppressed MBP68 - - 86-induced T cell proliferation compared to DC obtained at other time points in EAE and FCA-immunized rats. DC-derived NO induced apoptosis of CD4+ T cells, thereby inhibiting autoreactive T cell responses. Besides IFN-gamma stimulation, NO production by DC was mainly induced in an antigen-dependent manner when DC were co-cultured with T cells. The results suggest that spontaneous recovery from EAE is associated with augmented DC functions. Overproduction of NO by DC results in apoptosis of autoreactive CD4+ T cells, thereby decreasing autoreactive T cell reactivities. The existence of such a NO negative feedback loop may contribute to remission of EAE.

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 available

Pub Type(s)

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

Language

eng

PubMed ID

10408975

Citation

Xiao, B G., et al. "Mechanisms of Recovery From Experimental Allergic Encephalomyelitis Induced With Myelin Basic Protein Peptide 68-86 in Lewis Rats: a Role for Dendritic Cells in Inducing Apoptosis of CD4+ T Cells." Journal of Neuroimmunology, vol. 97, no. 1-2, 1999, pp. 25-36.
Xiao BG, Huang YM, Xu LY, et al. Mechanisms of recovery from experimental allergic encephalomyelitis induced with myelin basic protein peptide 68-86 in Lewis rats: a role for dendritic cells in inducing apoptosis of CD4+ T cells. J Neuroimmunol. 1999;97(1-2):25-36.
Xiao, B. G., Huang, Y. M., Xu, L. Y., Ishikawa, M., & Link, H. (1999). Mechanisms of recovery from experimental allergic encephalomyelitis induced with myelin basic protein peptide 68-86 in Lewis rats: a role for dendritic cells in inducing apoptosis of CD4+ T cells. Journal of Neuroimmunology, 97(1-2), 25-36.
Xiao BG, et al. Mechanisms of Recovery From Experimental Allergic Encephalomyelitis Induced With Myelin Basic Protein Peptide 68-86 in Lewis Rats: a Role for Dendritic Cells in Inducing Apoptosis of CD4+ T Cells. J Neuroimmunol. 1999 Jun 1;97(1-2):25-36. PubMed PMID: 10408975.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanisms of recovery from experimental allergic encephalomyelitis induced with myelin basic protein peptide 68-86 in Lewis rats: a role for dendritic cells in inducing apoptosis of CD4+ T cells. AU - Xiao,B G, AU - Huang,Y M, AU - Xu,L Y, AU - Ishikawa,M, AU - Link,H, PY - 1999/7/17/pubmed PY - 2000/6/1/medline PY - 1999/7/17/entrez SP - 25 EP - 36 JF - Journal of neuroimmunology JO - J. Neuroimmunol. VL - 97 IS - 1-2 N2 - Spontaneous remission of experimental allergic encephalomyelitis (EAE) is usually associated with prominent apoptosis. The mechanisms behind apoptosis are unknown. We examined the functions of dendritic cells (DC) from Lewis rats with EAE induced by immunization with myelin basic protein peptide 68-86 (MBP68 - - 86). Recovery from EAE was associated with three major functional changes of freshly prepared DC: (1) elevated proliferation, (2) increased nitric oxide (NO) production, and (3) augmented IFN-gamma secretion. In Freund's complete adjuvant (FCA)-immunized control rats, no increase of proliferation, NO production or IFN-gamma secretion was observed on day 21 post-immunization (p.i.), i.e., recovery from EAE. In vitro effects of IFN-gamma, TNF-alpha, TGF-beta1, IL-4 and IL-10 on DC were examined. IFN-gamma enhanced proliferation and NO production by DC, while TNF-alpha and IL-4 induced only slight DC proliferation. DC from recovering EAE rats (day 21 p.i.) suppressed MBP68 - - 86-induced T cell proliferation compared to DC obtained at other time points in EAE and FCA-immunized rats. DC-derived NO induced apoptosis of CD4+ T cells, thereby inhibiting autoreactive T cell responses. Besides IFN-gamma stimulation, NO production by DC was mainly induced in an antigen-dependent manner when DC were co-cultured with T cells. The results suggest that spontaneous recovery from EAE is associated with augmented DC functions. Overproduction of NO by DC results in apoptosis of autoreactive CD4+ T cells, thereby decreasing autoreactive T cell reactivities. The existence of such a NO negative feedback loop may contribute to remission of EAE. SN - 0165-5728 UR - https://www.unboundmedicine.com/medline/citation/10408975/Mechanisms_of_recovery_from_experimental_allergic_encephalomyelitis_induced_with_myelin_basic_protein_peptide_68_86_in_Lewis_rats:_a_role_for_dendritic_cells_in_inducing_apoptosis_of_CD4+_T_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0165-5728(99)00041-7 DB - PRIME DP - Unbound Medicine ER -