In vivo expansion of HLA-B35 alloreactive T cells sharing homologous T cell receptors: evidence for maintenance of an oligoclonally dominated allospecificity by persistent stimulation with an autologous MHC/peptide complex
In vivo expansion of HLA-B35 alloreactive T cells sharing homologous T cell receptors: evidence for maintenance of an oligoclonally dominated allospecificity by persistent stimulation with an autologous MHC/peptide complex
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共享同源 T 细胞受体的 HLA-B35 同种反应性 T 细胞的体内扩增:通过自体 MHC/肽复合物持续刺激维持寡克隆主导的同种异体特异性的证据
DOI:
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发表时间:
1995
影响因子:
15.3
通讯作者:
Dolores J. Schendel
中科院分区:
文献类型:
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作者:
Alexander Steinle;Carsten Reinhardt;Petra Jantzer;Dolores J. Schendel
The nature of alloantigens seen by T lymphocytes, in particular the role of peptides in allorecognition, has been studied intensively whereas knowledge about the in vivo emergence, diversity, and the structural basis of specificity of alloreactive T cells is very limited. Here we describe human T cell clones that recognize HLA-B35 alloantigens in a peptide-dependent manner. TCR sequence analysis revealed that several of these allospecific clones utilize homologous TCR: they all express TCRAV2S3J36C1 and TCRBV4S1J2S7C2 chains with highly related CDR3 sequences. Thus peptide-specific alloreactivity is reflected in homologous CDR3 sequences in a manner similar to that described for T cells that recognize nominal peptide/self-MHC complexes. The in vivo frequency of this TCR specificity was studied in unstimulated PBL of the responding cell donor who was not sensitized against HLA-B35. The vast majority (approximately 75%) of the VA2S3J36 junctional regions obtained from two samples of PBL, isolated at a 9-yr interval, encode CDR3 identical or homologous to those of the functionally characterized HLA-B35 allospecific T cells. These data are most easily explained by a model of alloreactivity in which persistent or recurrent exposure to a foreign peptide/self-MHC complex led to the in vivo expansion and long-term maintenance of specific T cells that show fortuitous crossrecognition of an HLA-B35/peptide complex and dominate the alloresponse against HLA-B35.
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影响因子:
56.9
作者:
HUNT, DF;HENDERSON, RA;ENGELHARD, VH
通讯作者:
ENGELHARD, VH
DOI:
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发表时间:
1989
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Shimizu,Y;DeMars,R
通讯作者:
DeMars,R
DOI:
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发表时间:
1989
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Miceli,MC;Finn,OJ
通讯作者:
Finn,OJ
DOI:
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发表时间:
1991
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Geiger,MJ;Gorski,J;Eckels,DD
通讯作者:
Eckels,DD