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Neonatal exposure of TCR BV8S2 transgenic mice to recombinant TCR BV8S2 results in reduced T cell proliferation and elevated antibody response to BV8S2, and increased severity of EAE.
J Neurosci Res 1998; 52(6):750-6JN

Abstract

Transgenic (Tg) mouse models are unique tools for investigating regulatory mechanisms of the immune system. Mice bearing a T cell receptor (TCR) BV8S2 transgene derived from an encephalitogenic T cell clone are highly susceptible to experimental autoimmune encephalomyelitis (EAE), a T cell-mediated neurological disorder. Although the pathogenesis of EAE is not yet fully understood, TCR-specific regulatory T cells seem to play a role in its remission and/or recovery process. In previous studies, we showed that immunization of BV8S2 Tg mice with recombinant BV8S2 protein induced TCR-specific T cells and protection against EAE, clearly indicating the persistence of a functional TCR regulatory network in spite of the highly skewed T cell repertoire. To further investigate the natural regulatory role of TCR-specific T cells, we evaluated the effect on EAE of inducing neonatal tolerance to heterologous (rat) and homologous BV8S2 proteins in Tg mice. Neonatal exposure to rat BV8S2 protein induced "split" tolerance, characterized by decreased T cell proliferation but increased antibody responses to both rat and mouse BV8S2 proteins that are known to be cross-reactive. When challenged as adults with an encephalitogenic emulsion, Tg mice tolerized with rat but not mouse BV8S2 protein developed more severe EAE compared to control mice. These results demonstrate that immunity to BV8S2 determinants in BV8S2 Tg mice is naturally induced and functions to limit the severity of EAE.

Authors+Show Affiliations

Biogal Pharmaceutical, Debrecen, Hungary.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

9669324

Citation

Siklodi, B, et al. "Neonatal Exposure of TCR BV8S2 Transgenic Mice to Recombinant TCR BV8S2 Results in Reduced T Cell Proliferation and Elevated Antibody Response to BV8S2, and Increased Severity of EAE." Journal of Neuroscience Research, vol. 52, no. 6, 1998, pp. 750-6.
Siklodi B, Jacobs R, Vandenbark AA, et al. Neonatal exposure of TCR BV8S2 transgenic mice to recombinant TCR BV8S2 results in reduced T cell proliferation and elevated antibody response to BV8S2, and increased severity of EAE. J Neurosci Res. 1998;52(6):750-6.
Siklodi, B., Jacobs, R., Vandenbark, A. A., & Offner, H. (1998). Neonatal exposure of TCR BV8S2 transgenic mice to recombinant TCR BV8S2 results in reduced T cell proliferation and elevated antibody response to BV8S2, and increased severity of EAE. Journal of Neuroscience Research, 52(6), pp. 750-6.
Siklodi B, et al. Neonatal Exposure of TCR BV8S2 Transgenic Mice to Recombinant TCR BV8S2 Results in Reduced T Cell Proliferation and Elevated Antibody Response to BV8S2, and Increased Severity of EAE. J Neurosci Res. 1998 Jun 15;52(6):750-6. PubMed PMID: 9669324.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neonatal exposure of TCR BV8S2 transgenic mice to recombinant TCR BV8S2 results in reduced T cell proliferation and elevated antibody response to BV8S2, and increased severity of EAE. AU - Siklodi,B, AU - Jacobs,R, AU - Vandenbark,A A, AU - Offner,H, PY - 1998/7/21/pubmed PY - 2000/6/20/medline PY - 1998/7/21/entrez SP - 750 EP - 6 JF - Journal of neuroscience research JO - J. Neurosci. Res. VL - 52 IS - 6 N2 - Transgenic (Tg) mouse models are unique tools for investigating regulatory mechanisms of the immune system. Mice bearing a T cell receptor (TCR) BV8S2 transgene derived from an encephalitogenic T cell clone are highly susceptible to experimental autoimmune encephalomyelitis (EAE), a T cell-mediated neurological disorder. Although the pathogenesis of EAE is not yet fully understood, TCR-specific regulatory T cells seem to play a role in its remission and/or recovery process. In previous studies, we showed that immunization of BV8S2 Tg mice with recombinant BV8S2 protein induced TCR-specific T cells and protection against EAE, clearly indicating the persistence of a functional TCR regulatory network in spite of the highly skewed T cell repertoire. To further investigate the natural regulatory role of TCR-specific T cells, we evaluated the effect on EAE of inducing neonatal tolerance to heterologous (rat) and homologous BV8S2 proteins in Tg mice. Neonatal exposure to rat BV8S2 protein induced "split" tolerance, characterized by decreased T cell proliferation but increased antibody responses to both rat and mouse BV8S2 proteins that are known to be cross-reactive. When challenged as adults with an encephalitogenic emulsion, Tg mice tolerized with rat but not mouse BV8S2 protein developed more severe EAE compared to control mice. These results demonstrate that immunity to BV8S2 determinants in BV8S2 Tg mice is naturally induced and functions to limit the severity of EAE. SN - 0360-4012 UR - https://www.unboundmedicine.com/medline/citation/9669324/Neonatal_exposure_of_TCR_BV8S2_transgenic_mice_to_recombinant_TCR_BV8S2_results_in_reduced_T_cell_proliferation_and_elevated_antibody_response_to_BV8S2_and_increased_severity_of_EAE_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0360-4012&date=1998&volume=52&issue=6&spage=750 DB - PRIME DP - Unbound Medicine ER -