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Experimental autoimmune encephalomyelitis-resistant mice have highly encephalitogenic myelin basic protein (MBP)-specific T cell clones that recognize a MBP peptide with high affinity for MHC class II.
J Immunol. 1995 Jan 01; 154(1):388-98.JI

Abstract

BALB/c mice are resistant to disease induction when experimental protocols that induce experimental autoimmune encephalomyelitis (EAE) in susceptible strains of animals are used. We have previously described a panel of myelin basic protein (MBP)-specific CD4+ T cell clones from BALB/c mice, two of which induce moderate EAE when transferred to syngeneic recipients. These clones are I-E(d) restricted and recognize residues 151-160 of mouse MBP. Here, we describe a series of 17 MBP-reactive T cell clones, which were derived from two BALB/c mice. All are I-A(d) restricted and recognize nested epitopes in peptide 59-76 of mouse MBP. Four different TCR V beta chains are used by this panel of clones; these include V beta 8.2 (10/17), V beta 8.1 (2/17), V beta 7 (3/17), and V beta 14 (2/17). Twelve of fourteen clones tested adoptively transferred severe demyelinating EAE to syngeneic recipients. Studies of relative binding affinities of MBP peptides to class II molecules I-A(d) and I-E(d) show that peptide 59-76 binds with extremely high affinity to I-A(d), whereas three peptides that contains residues 151-160 bind poorly to I-E(d). These results are consistent with a growing number of reports that show that high affinity binding to class II is required for autoantigenic stimulation. Despite encephalitogenicity of 59-76-reactive T cells, active immunization of BALB/c mice with peptide 59-76 in adjuvant failed to induce either clinical or histologic signs of EAE. The implications of these findings for mechanisms of genetically determined EAE resistance are discussed.

Authors+Show Affiliations

Department of Pathology, Harvard Medical School, Boston, MA 02115.No 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
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

7527816

Citation

Abromson-Leeman, S, et al. "Experimental Autoimmune Encephalomyelitis-resistant Mice Have Highly Encephalitogenic Myelin Basic Protein (MBP)-specific T Cell Clones That Recognize a MBP Peptide With High Affinity for MHC Class II." Journal of Immunology (Baltimore, Md. : 1950), vol. 154, no. 1, 1995, pp. 388-98.
Abromson-Leeman S, Alexander J, Bronson R, et al. Experimental autoimmune encephalomyelitis-resistant mice have highly encephalitogenic myelin basic protein (MBP)-specific T cell clones that recognize a MBP peptide with high affinity for MHC class II. J Immunol. 1995;154(1):388-98.
Abromson-Leeman, S., Alexander, J., Bronson, R., Carroll, J., Southwood, S., & Dorf, M. (1995). Experimental autoimmune encephalomyelitis-resistant mice have highly encephalitogenic myelin basic protein (MBP)-specific T cell clones that recognize a MBP peptide with high affinity for MHC class II. Journal of Immunology (Baltimore, Md. : 1950), 154(1), 388-98.
Abromson-Leeman S, et al. Experimental Autoimmune Encephalomyelitis-resistant Mice Have Highly Encephalitogenic Myelin Basic Protein (MBP)-specific T Cell Clones That Recognize a MBP Peptide With High Affinity for MHC Class II. J Immunol. 1995 Jan 1;154(1):388-98. PubMed PMID: 7527816.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Experimental autoimmune encephalomyelitis-resistant mice have highly encephalitogenic myelin basic protein (MBP)-specific T cell clones that recognize a MBP peptide with high affinity for MHC class II. AU - Abromson-Leeman,S, AU - Alexander,J, AU - Bronson,R, AU - Carroll,J, AU - Southwood,S, AU - Dorf,M, PY - 1995/1/1/pubmed PY - 1995/1/1/medline PY - 1995/1/1/entrez SP - 388 EP - 98 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 154 IS - 1 N2 - BALB/c mice are resistant to disease induction when experimental protocols that induce experimental autoimmune encephalomyelitis (EAE) in susceptible strains of animals are used. We have previously described a panel of myelin basic protein (MBP)-specific CD4+ T cell clones from BALB/c mice, two of which induce moderate EAE when transferred to syngeneic recipients. These clones are I-E(d) restricted and recognize residues 151-160 of mouse MBP. Here, we describe a series of 17 MBP-reactive T cell clones, which were derived from two BALB/c mice. All are I-A(d) restricted and recognize nested epitopes in peptide 59-76 of mouse MBP. Four different TCR V beta chains are used by this panel of clones; these include V beta 8.2 (10/17), V beta 8.1 (2/17), V beta 7 (3/17), and V beta 14 (2/17). Twelve of fourteen clones tested adoptively transferred severe demyelinating EAE to syngeneic recipients. Studies of relative binding affinities of MBP peptides to class II molecules I-A(d) and I-E(d) show that peptide 59-76 binds with extremely high affinity to I-A(d), whereas three peptides that contains residues 151-160 bind poorly to I-E(d). These results are consistent with a growing number of reports that show that high affinity binding to class II is required for autoantigenic stimulation. Despite encephalitogenicity of 59-76-reactive T cells, active immunization of BALB/c mice with peptide 59-76 in adjuvant failed to induce either clinical or histologic signs of EAE. The implications of these findings for mechanisms of genetically determined EAE resistance are discussed. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/7527816/Experimental_autoimmune_encephalomyelitis_resistant_mice_have_highly_encephalitogenic_myelin_basic_protein__MBP__specific_T_cell_clones_that_recognize_a_MBP_peptide_with_high_affinity_for_MHC_class_II_ L2 - https://www.jimmunol.org/lookup/pmidlookup?view=long&pmid=7527816 DB - PRIME DP - Unbound Medicine ER -