Disease relevance of Genes, T-Cell Receptor gamma

• The spleen in case 1 was positive for Epstein-Barr virus genome and showed TCR-gamma gene rearrangement by polymerase chain reaction [1].
• Analysis of the nucleotide sequences of the rearranged T-cell receptor gamma-chain (TCR-gamma) gene revealed that this lineage switch resulted from the selection of the T-lineage subclone in SCID mice, which had expanded at onset [2].

High impact information on Genes, T-Cell Receptor gamma

• Several recent studies have identified a distinct subset of CD3(T3)+CD4-CD8-T lymphocytes that express a CD3-associated heterodimer made up of the protein encoded by the T-cell receptor (TCR) gamma-gene and a second glycoprotein termed TCR delta (refs 1-4) [3].
• Evidence indicates that this biased developmental potential is not a result of enhanced TCR-gamma gene rearrangement/expression in IL-7R(+) pro-T cells [4].
• The expression of the murine TCR-gamma genes was examined in a series of IL-3-dependent and growth factor-independent cell lines [5].
• TCR gamma repertoire diversification was initiated on embryonic day 10 by an apparently random pattern of V-J gamma recombination, nuclease activity, and P-and N-nucleotide additions to generate a diverse repertoire of avian TCR gamma genes early in ontogeny [6].
• Induction of myeloid differentiation in these cells clones down expression and/or transcriptional accessibility of the immunoglobulin heavy-chain and TCR gamma genes [7].

Biological context of Genes, T-Cell Receptor gamma

• CONCLUSION: Inconclusive histology is probably a heterogeneous group in which CD7 counts and TCR gamma gene rearrangement studies might help to differentiate the MF cases from the benign cases [8].
• Molecular biology studies of immunomagnetically fractionated cells using a T gamma 9 TCR gamma gene primer further revealed that the CD4+ and CD8+ components were both clonal but showed different patterns of rearrangement [9].
• T-cell receptor (TCR) gene analysis was performed on blood and tissue samples using polymerase chain reaction/single-strand conformational polymorphism analysis of the TCR-gamma gene using consensus primers [10].
• T cell receptor gamma (TCR-gamma) and immunoglobulin heavy chain (IgH) gene rearrangements were assayed using our standard clinical polymerase chain reaction procedures targeting each of the four functional variable (V) families and the three joining (J) families of the TCR-gamma gene, and framework III of the IgH gene, respectively [11].
• AD genes were mapped near the FC epsilon RI beta gene (around D11S1314 locus) on chromosome 11, the IL4 gene cluster on chromosome 5 and the TCR gamma gene on chromosome 7 [12].

Anatomical context of Genes, T-Cell Receptor gamma

• Treatment of IL-7Ralpha-/- precursor T cells with the specific histone deacetylase inhibitor trichostatin A released the block of TCR-gamma gene rearrangement [13].
• We report here that YS cells grown in short-term cell culture show no detectable rearrangement or transcription at the TcR gamma gene locus, although the TcR gamma gene of in vitro transformed YS cells rearranges in the absence of the thymus [14].
• Murine IL-3-dependent myeloid cell lines express transcripts from non-rearranged TCR gamma genes and this expression is dependent upon IL-3 [15].

Associations of Genes, T-Cell Receptor gamma with chemical compounds

• Mutant T-lymphocytes with rearranged TCR gamma genes containing the same V and J subgroups were analyzed using PCR-based denaturing polyacrylamide gel electrophoresis [16].
• The data presented here suggest that TCR gamma gene rearrangement in adult pre-T cells is regulated by IL-7, but that the TCR beta locus requires additional or alternative signals for the induction of complete rearrangement [17].
• The MNNG-exposed Bloom syndrome (BS) B-lymphoblastoid cell population (BS-MNNG), when analyzed for aberrant genetic variations, showed an illegitimate rearrangement at the TCR-gamma gene and hypermethylation at the c-myb protooncogene [18].

Gene context of Genes, T-Cell Receptor gamma

• The results demonstrate that IL-7R-mediated signals are necessary for the normal expression of rearranged TCR-gamma genes [19].
• To investigate this observation in general terms we examined various IL-3 dependent cell lines for TCR gamma gene expression [15].
• 32D cells transfected with the IL-2 beta chain receptor became responsive to IL-2 as a growth factor and induced TCR gamma gene expression [15].
• Specificity for detection of an EITCL using immunohistology was 77% for CD8 and for TCR-beta staining, and 100% for detection of a clonal TCR-gamma gene rearrangement [20].
• We postulate that there is an evolutionary chromosomal breakpoint between the bg gene and the TCR-gamma gene [21].

References