A mouse T lymphoma that lacks T-cell receptor surface expression exhibits allelic exclusion of its ? chain genes

Mori, Lucia; Ricciardi‐Castagnoli, Paola; Steinmetz, Michael

doi:10.1007/bf00346161

Cited by 3 publications

(1 citation statement)

References 29 publications

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“…Although two or three identical amino acids may arise by chance in functionally diverse CDR3 sequences, the shared LG(G/A)NQD sequence noted here is likely to be rare. Indeed a computer search of the 488 mouse TCR sequences and the 1015 human TCR sequences present in the GenPep library (up-dated through July 1997) yielded no sequences identical to either LGGNQD or LGANQD, and only one sequence with one mismatch: I in place of either G or A, detected in a lymphoma cell (17).…”

Section: Discussionmentioning

confidence: 99%

A shared TCR CDR3 sequence in NOD mouse autoimmune diabetes

Tikochinski

Elias²,

Steeg³

et al. 1999

International Immunology

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T cells involved in autoimmune diseases have been characterized by the genetic elements used to construct their autoimmune TCR. In the present study, we sequenced the alpha and beta chains of the TCR expressed by a CD4(+) T cell clone, C9, functional in NOD mouse diabetes. Clone C9 can adoptively transfer diabetes or, when attenuated, C9 can be used to vaccinate NOD mice against diabetes. Clone C9 recognizes a peptide epitope (p277) of the 60 kDa heat shock protein (hsp60) molecule. We now report that the C9 TCR beta chain features a CDR3 peptide sequence that is prevalent among NOD mice. This CDR3 element is detectable by 2 weeks of age in the thymus, and later in the spleen and in the autoimmune insulitis. Thus, a TCR CDR3beta sequence appears to be a common idiotope associated with mouse diabetes.

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Section: Discussionmentioning

confidence: 99%

A shared TCR CDR3 sequence in NOD mouse autoimmune diabetes

Tikochinski

Elias²,

Steeg³

et al. 1999

International Immunology

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Human T-cell receptor variable gene segment families

et al. 1995

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Multiple DNA and protein sequence alignments have been constructed for the human T-cell receptor cVS, [3, and y (TCRA/D, B, and G) variable (V) gene segments. The traditional classification into subfamilies was confirmed using a much larger pool of sequences. For each sequence, a name was derived which complies with the standard nomenclature. The traditional numbering of V gene segments in the order of their discovery was continued and changed when in conflict with names of other segments_ By discriminating between alleles at the same locus versus genes from different loci, we were able to reduce the number of more than 150 different TCRBV sequences in the database to a repertoire of only 47 functional TCRBV gene segments. An extension of this analysis to the over 1 O0 TCRAV sequences results in a predicted repertoire of 42 functional TCRAV gene segments. Our alignment revealed two residues that distinguish between the highly homologous V8 and Vo~ one at a site that in VH contacts the constant region, the other at the interface between immunoglobulin Vn and VL. This site may be responsible for restricted pairing between certain V8 and Vy chains. On the other hand, V[3 and V 7 appear to be related by the fact that their CDR2 length is increased by four residues as compared with that of VcV8 peptides.The alignment data reported in this paper have been submitted to the EMBL nucleotide sequence database and have been assigned the alignment number DS23485. The data are available by the EBI FTP server and file server

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An erythroid specific enhancer upstream to the gene encodin the cell-type specific transcription factor GATA-1

Nicolis

Bertini²,

Ronchi³

et al. 1991

Nucl Acids Res

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The transcription factor GATA-1 is expressed in a subset of hemopoietic cells, where it mediates the cell-type specific expression of several genes. We have cloned the mouse and human GATA-1 genes. A region upstream to the first exon, and highly conserved between mouse and man, acts as an erythroid specific enhancer in transient assays, if linked to the GATA-1 or to the SV40 promoter. The activity of the enhancer is almost completely dependent on the integrity of a dimeric GATA-1 binding site.

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A mouse T lymphoma that lacks T-cell receptor surface expression exhibits allelic exclusion of its ? chain genes

Cited by 3 publications

References 29 publications

A shared TCR CDR3 sequence in NOD mouse autoimmune diabetes

A shared TCR CDR3 sequence in NOD mouse autoimmune diabetes

Human T-cell receptor variable gene segment families

An erythroid specific enhancer upstream to the gene encodin the cell-type specific transcription factor GATA-1

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