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Essential role of TGF-beta in the natural resistance to experimental allergic encephalomyelitis in rats.
Eur J Immunol. 2001 Apr; 31(4):1132-40.EJ

Abstract

Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease induced in susceptible rat strains by a single immunization with myelin basic protein (MBP). The Lewis (LEW) strain is susceptible to disease induction while the Brown Norway (BN) strain is resistant. This resistance involves non-MHC genes since congenic BN-1L rats, with LEW MHC on a BN-derived background, are also resistant. In the present study we show that, upon immunization with MBP, the non-MHC-encoded resistance to develop clinical EAE in BN-1L rats is associated with a decreased production of IFN-gamma. This may be due to a difference between LEW and BN-1L rats in their ability to produce regulatory cytokines such as IL-4, IL-10 and TGF-beta. In comparison to LEW rats, immune lymph node cells from BN-1L rats express an increased amount of IL-4 mRNA but produce less IL-10. Furthermore, the sera from BN-1L rats contain higher amounts of active TGF-beta1. Therefore, we have investigated the involvement of IL-4 and TGF-beta in the resistance of BN-1L rats to develop EAE using neutralizing mAb. Neutralization of TGF-beta, but not IL-4, renders BN-1L rats susceptible to clinical EAE without affecting the proliferation or the cytokine repertoire of immune lymph node cells. With respect to the origin of the endogenous TGF-beta production, we excluded the involvement of CD8 T cells and discuss a possible role of platelets and of CD4 T cells exhibiting the CD45RC(low) phenotype.

Authors+Show Affiliations

INSERM U28, Institut Fédératif de recherche 30, and Université Paul Sabatier, Toulouse, France.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

11298338

Citation

Cautain, B, et al. "Essential Role of TGF-beta in the Natural Resistance to Experimental Allergic Encephalomyelitis in Rats." European Journal of Immunology, vol. 31, no. 4, 2001, pp. 1132-40.
Cautain B, Damoiseaux J, Bernard I, et al. Essential role of TGF-beta in the natural resistance to experimental allergic encephalomyelitis in rats. Eur J Immunol. 2001;31(4):1132-40.
Cautain, B., Damoiseaux, J., Bernard, I., van Straaten, H., van Breda Vriesman, P., Boneu, B., Druet, P., & Saoudi, A. (2001). Essential role of TGF-beta in the natural resistance to experimental allergic encephalomyelitis in rats. European Journal of Immunology, 31(4), 1132-40.
Cautain B, et al. Essential Role of TGF-beta in the Natural Resistance to Experimental Allergic Encephalomyelitis in Rats. Eur J Immunol. 2001;31(4):1132-40. PubMed PMID: 11298338.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Essential role of TGF-beta in the natural resistance to experimental allergic encephalomyelitis in rats. AU - Cautain,B, AU - Damoiseaux,J, AU - Bernard,I, AU - van Straaten,H, AU - van Breda Vriesman,P, AU - Boneu,B, AU - Druet,P, AU - Saoudi,A, PY - 2001/4/12/pubmed PY - 2001/5/22/medline PY - 2001/4/12/entrez SP - 1132 EP - 40 JF - European journal of immunology JO - Eur. J. Immunol. VL - 31 IS - 4 N2 - Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease induced in susceptible rat strains by a single immunization with myelin basic protein (MBP). The Lewis (LEW) strain is susceptible to disease induction while the Brown Norway (BN) strain is resistant. This resistance involves non-MHC genes since congenic BN-1L rats, with LEW MHC on a BN-derived background, are also resistant. In the present study we show that, upon immunization with MBP, the non-MHC-encoded resistance to develop clinical EAE in BN-1L rats is associated with a decreased production of IFN-gamma. This may be due to a difference between LEW and BN-1L rats in their ability to produce regulatory cytokines such as IL-4, IL-10 and TGF-beta. In comparison to LEW rats, immune lymph node cells from BN-1L rats express an increased amount of IL-4 mRNA but produce less IL-10. Furthermore, the sera from BN-1L rats contain higher amounts of active TGF-beta1. Therefore, we have investigated the involvement of IL-4 and TGF-beta in the resistance of BN-1L rats to develop EAE using neutralizing mAb. Neutralization of TGF-beta, but not IL-4, renders BN-1L rats susceptible to clinical EAE without affecting the proliferation or the cytokine repertoire of immune lymph node cells. With respect to the origin of the endogenous TGF-beta production, we excluded the involvement of CD8 T cells and discuss a possible role of platelets and of CD4 T cells exhibiting the CD45RC(low) phenotype. SN - 0014-2980 UR - https://www.unboundmedicine.com/medline/citation/11298338/Essential_role_of_TGF_beta_in_the_natural_resistance_to_experimental_allergic_encephalomyelitis_in_rats_ DB - PRIME DP - Unbound Medicine ER -