TY - JOUR
T1 - A TCR Vα CDR3-specific motif associated with lewis rat autoimmune encephalomyelitis and basic protein-specific T cell clones
AU - Buenafe, Abigail C.
AU - Tsu, Rachel C.
AU - Bebo, Bruce
AU - Bakke, Antony C.
AU - Vandenbark, Arthur A.
AU - Offner, Halina
N1 - Copyright:
Copyright 2005 Elsevier Science B.V., Amsterdam. All rights reserved.
PY - 1997
Y1 - 1997
N2 - To investigate TCR Vα gene expression in the Lewis rat model of experimental autoimmune encephalomyelitis, we obtained Vα chain sequences from two Vβ8.2-encephalitogenic, BP72-89-specific T cell clones. Two different Vα genes, a Vα2 gene and a Vα23 gene, are utilized, but both were found to contain an asparagine repeat (Asn3+) sequence present in the Vα CDR3 region. This Asn3+ motif is also present in the previously reported sequence of a BP68-88-specific hybridoma, 510, which utilizes a different Vα2 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 Vα expression in the OX-40+ population revealed the biased use of three Vα genes, Vα1, Vα2, and Vα23. The Asn3+ motif was present in the Vα CDR3 region of Vα1, Vα2, and Vα23 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 Vα chain sequences are nearly identical to those utilized by the BP-specific encephalitogenic clones described, it is likely that these Vα sequences are derived from disease-associated T cells in the spinal cord. Thus, we demonstrate that the Asn3+ Vα 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.
AB - To investigate TCR Vα gene expression in the Lewis rat model of experimental autoimmune encephalomyelitis, we obtained Vα chain sequences from two Vβ8.2-encephalitogenic, BP72-89-specific T cell clones. Two different Vα genes, a Vα2 gene and a Vα23 gene, are utilized, but both were found to contain an asparagine repeat (Asn3+) sequence present in the Vα CDR3 region. This Asn3+ motif is also present in the previously reported sequence of a BP68-88-specific hybridoma, 510, which utilizes a different Vα2 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 Vα expression in the OX-40+ population revealed the biased use of three Vα genes, Vα1, Vα2, and Vα23. The Asn3+ motif was present in the Vα CDR3 region of Vα1, Vα2, and Vα23 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 Vα chain sequences are nearly identical to those utilized by the BP-specific encephalitogenic clones described, it is likely that these Vα sequences are derived from disease-associated T cells in the spinal cord. Thus, we demonstrate that the Asn3+ Vα 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.
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M3 - Article
C2 - 9164970
AN - SCOPUS:0031155388
SN - 0022-1767
VL - 158
SP - 5472
EP - 5483
JO - Journal of Immunology
JF - Journal of Immunology
IS - 11
ER -