Tags

Type your tag names separated by a space and hit enter

A TCR V alpha CDR3-specific motif associated with Lewis rat autoimmune encephalomyelitis and basic protein-specific T cell clones.
J Immunol. 1997 Jun 01; 158(11):5472-83.JI

Abstract

To investigate TCR V alpha gene expression in the Lewis rat model of experimental autoimmune encephalomyelitis, we obtained V alpha chain sequences from two V beta8.2+-encephalitogenic, BP72-89-specific T cell clones. Two different V alpha genes, a V alpha2 gene and a V alpha23 gene, are utilized, but both were found to contain an asparagine repeat (Asn3+) sequence present in the V alpha CDR3 region. This Asn3+ motif is also present in the previously reported sequence of a BP68-88-specific hybridoma, 510, which utilizes a different V alpha2 gene family member. In further experiments, spinal cord T cells were isolated at the onset of basic protein (BP)-induced disease and sorted for the OX-40 activation marker, which we have previously used to enrich for specifically activated T cells. Analysis of V alpha expression in the OX-40+ population revealed the biased use of three V alpha genes, V alpha1, V alpha2, and V alpha23. The Asn3+ motif was present in the V alpha CDR3 region of V alpha1, V alpha2, and V alpha23 cDNA derived from OX-40+ spinal cord T cells but found to be generally absent in the OX-40- spinal cord population. Since these Asn3+ motif-bearing V alpha chain sequences are nearly identical to those utilized by the BP-specific encephalitogenic clones described, it is likely that these V alpha sequences are derived from disease-associated T cells in the spinal cord. Thus, we demonstrate that the Asn3+ V alpha CDR3 motif is strongly associated with experimental autoimmune encephalomyelitis in the Lewis rat and propose that it plays a role in TCR recognition of a specific BP peptide/MHC complex.

Authors+Show Affiliations

Department of Neurology, Oregon Health Sciences University, Portland 97201, USA.No affiliation info availableNo affiliation info availableNo 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

9164970

Citation

Buenafe, A C., et al. "A TCR V Alpha CDR3-specific Motif Associated With Lewis Rat Autoimmune Encephalomyelitis and Basic Protein-specific T Cell Clones." Journal of Immunology (Baltimore, Md. : 1950), vol. 158, no. 11, 1997, pp. 5472-83.
Buenafe AC, Tsu RC, Bebo B, et al. A TCR V alpha CDR3-specific motif associated with Lewis rat autoimmune encephalomyelitis and basic protein-specific T cell clones. J Immunol. 1997;158(11):5472-83.
Buenafe, A. C., Tsu, R. C., Bebo, B., Bakke, A. C., Vandenbark, A. A., & Offner, H. (1997). A TCR V alpha CDR3-specific motif associated with Lewis rat autoimmune encephalomyelitis and basic protein-specific T cell clones. Journal of Immunology (Baltimore, Md. : 1950), 158(11), 5472-83.
Buenafe AC, et al. A TCR V Alpha CDR3-specific Motif Associated With Lewis Rat Autoimmune Encephalomyelitis and Basic Protein-specific T Cell Clones. J Immunol. 1997 Jun 1;158(11):5472-83. PubMed PMID: 9164970.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A TCR V alpha CDR3-specific motif associated with Lewis rat autoimmune encephalomyelitis and basic protein-specific T cell clones. AU - Buenafe,A C, AU - Tsu,R C, AU - Bebo,B,Jr AU - Bakke,A C, AU - Vandenbark,A A, AU - Offner,H, PY - 1997/6/1/pubmed PY - 2001/3/28/medline PY - 1997/6/1/entrez SP - 5472 EP - 83 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 158 IS - 11 N2 - To investigate TCR V alpha gene expression in the Lewis rat model of experimental autoimmune encephalomyelitis, we obtained V alpha chain sequences from two V beta8.2+-encephalitogenic, BP72-89-specific T cell clones. Two different V alpha genes, a V alpha2 gene and a V alpha23 gene, are utilized, but both were found to contain an asparagine repeat (Asn3+) sequence present in the V alpha CDR3 region. This Asn3+ motif is also present in the previously reported sequence of a BP68-88-specific hybridoma, 510, which utilizes a different V alpha2 gene family member. In further experiments, spinal cord T cells were isolated at the onset of basic protein (BP)-induced disease and sorted for the OX-40 activation marker, which we have previously used to enrich for specifically activated T cells. Analysis of V alpha expression in the OX-40+ population revealed the biased use of three V alpha genes, V alpha1, V alpha2, and V alpha23. The Asn3+ motif was present in the V alpha CDR3 region of V alpha1, V alpha2, and V alpha23 cDNA derived from OX-40+ spinal cord T cells but found to be generally absent in the OX-40- spinal cord population. Since these Asn3+ motif-bearing V alpha chain sequences are nearly identical to those utilized by the BP-specific encephalitogenic clones described, it is likely that these V alpha sequences are derived from disease-associated T cells in the spinal cord. Thus, we demonstrate that the Asn3+ V alpha CDR3 motif is strongly associated with experimental autoimmune encephalomyelitis in the Lewis rat and propose that it plays a role in TCR recognition of a specific BP peptide/MHC complex. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/9164970/A_TCR_V_alpha_CDR3_specific_motif_associated_with_Lewis_rat_autoimmune_encephalomyelitis_and_basic_protein_specific_T_cell_clones_ L2 - https://www.jimmunol.org/lookup/pmidlookup?view=long&pmid=9164970 DB - PRIME DP - Unbound Medicine ER -