Functional analysis of the murine T-cell receptor beta enhancer and characteristics of its DNA-binding proteins

1990 ◽  
Vol 10 (10) ◽  
pp. 5027-5035
Author(s):  
J Takeda ◽  
A Cheng ◽  
F Mauxion ◽  
C A Nelson ◽  
R D Newberry ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Lymphoid Cells ◽  
Mobility Shift ◽  
Enhancer Activity ◽  
Mobility Shift Assay ◽  
Gel Mobility Shift ◽  
Beta Enhancer

The minimal T-cell receptor (TCR) beta-chain (TCR beta) enhancer has been identified by transfection into lymphoid cells. The minimal enhancer was active in T cells and in some B-lineage cells. When a larger fragment containing the minimal enhancer was used, its activity was apparent only in T cells. Studies with phytohemagglutinin and 4 beta-phorbol-12,13-dibutyrate revealed that the enhancer activity was increased by these agents. By a combination of DNase I footprinting, gel mobility shift assay, and methylation interference analysis, seven different motifs were identified within the minimal enhancer. Furthermore, competition experiments showed that some of these elements bound identical or similar factors that are known to bind to the TCR V beta promoter decamer or to the immunoglobulin enhancer kappa E2 or muEBP-E motif. These shared motifs may be important in the differential gene activity among the different lymphoid subsets.

scholarly journals Functional analysis of the murine T-cell receptor beta enhancer and characteristics of its DNA-binding proteins.

1990 ◽  
Vol 10 (10) ◽  
pp. 5027-5035 ◽  
Author(s):  
J Takeda ◽  
A Cheng ◽  
F Mauxion ◽  
C A Nelson ◽  
R D Newberry ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Lymphoid Cells ◽  
Mobility Shift ◽  
Enhancer Activity ◽  
Mobility Shift Assay ◽  
Gel Mobility Shift ◽  
Beta Enhancer

The minimal T-cell receptor (TCR) beta-chain (TCR beta) enhancer has been identified by transfection into lymphoid cells. The minimal enhancer was active in T cells and in some B-lineage cells. When a larger fragment containing the minimal enhancer was used, its activity was apparent only in T cells. Studies with phytohemagglutinin and 4 beta-phorbol-12,13-dibutyrate revealed that the enhancer activity was increased by these agents. By a combination of DNase I footprinting, gel mobility shift assay, and methylation interference analysis, seven different motifs were identified within the minimal enhancer. Furthermore, competition experiments showed that some of these elements bound identical or similar factors that are known to bind to the TCR V beta promoter decamer or to the immunoglobulin enhancer kappa E2 or muEBP-E motif. These shared motifs may be important in the differential gene activity among the different lymphoid subsets.

scholarly journals Fetal liver T cell receptor gamma/delta+ T cells as cytotoxic T lymphocytes specific for maternal alloantigens.

1992 ◽  
Vol 176 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Y Miyagawa ◽  
T Matsuoka ◽  
A Baba ◽  
T Nakamura ◽  
T Tsuno ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Lines ◽  
Fetal Liver ◽  
Cell Receptor ◽  
Lymphoid Cells ◽  
Gamma Delta T Cells ◽  
Gamma Delta ◽  
Killer Activity

We have established fetal liver-derived T cell receptor (TCR) gamma/delta+, CD3+ T cell lines that are cytotoxic for maternal T cells. Fetal liver-derived lymphoid progenitors yielded predominantly TCR-gamma/delta+ cell clusters when cultured on fetal bone marrow-derived stromal cells in the presence of a cytokine cocktail under magnetic force. These tightly adherent clusters were cloned by limiting dilution and the resulting cell lines analyzed for phenotype and function. Six of eight TCR-gamma/delta lines from 8-9.5-wk gestation fetuses were V delta 2+ as compared with zero of eight lines from later stages of gestation (10 and 15 wk), where all the lines were V delta 1+. In cytotoxicity assays, these TCR-gamma/delta+, CD3+, CD4-, and CD8+ or CD8- long-term cultured lymphoid cells (LLC) were killer cells active against the class I antigens on maternal T cells. Of the cell lines, the CD8+ TCR-gamma/delta+ LLC had the highest levels of killer activity. Thus fetal liver TCR-gamma/delta+ T cells may play a crucial role in protection against invading maternal T cells generated in the feto-maternal interaction.

scholarly journals T-cell leukemias with rearrangement of the gamma but not beta T-cell receptor genes

Blood ◽  
1988 ◽  
Vol 71 (2) ◽  
pp. 356-362 ◽  
Author(s):  
L Foroni ◽  
E Matutes ◽  
J Foldi ◽  
R Morilla ◽  
T Rabbitts ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Lymphoid Cells ◽  
Leukemic Cells ◽  
New Information ◽  
Combined Use ◽  
T Cell Receptor Genes ◽  
Lgl Leukemia

Abstract beta and gamma T cell receptor (TCR) gene configuration was studied in 12 patients with large granular lymphocyte T cell leukemia (LGL- leukemia). Both genes were found rearranged in ten cases. In the remaining two patients TCR beta was found in germline configuration. In one of them rearrangement of T cell-rearranging gene gamma (TRG gamma) and a gamma mRNA were demonstrated. We suggest that in this patient the leukemic T cells arose from one of the rare T cells bearing a gamma- delta rather than an alpha-beta TCR heterodimeric molecule. In the other patient several discrete TRG gamma rearrangements were detected. Because her leukemic cells were shown to be monoclonal on the grounds of their karyotype, we suggest that her leukemia originated before any rearrangement had taken place. The combined use of TCR beta and TRG gamma probes provides new information on the origin and clonal expansion of lymphoid cells in LGL-leukemia.

GATA elements are necessary for the activity and tissue specificity of the T-cell receptor beta-chain transcriptional enhancer

1994 ◽  
Vol 14 (6) ◽  
pp. 4286-4294
Author(s):  
A J Henderson ◽  
S McDougall ◽  
J Leiden ◽  
K L Calame
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Beta Chain ◽  
Transcriptional Enhancer ◽  
T Cell Receptor Beta ◽  
Beta Enhancer ◽  
Receptor Beta

Three high-affinity binding sites for the GATA family of transcriptional regulators have been identified within the T-cell receptor beta-chain (TCR beta) transcriptional enhancer, and their functional significance has been determined in an effort to understand the T-cell specificity of the enhancer more fully. One site, TE4, is important for activity of the enhancer in T cells. Neither site TE1 nor site TE2 can functionally replace a mutated TE4 site in T cells; however, the same protein, probably GATA-3, binds all three sites, as judged by electrophoretic mobility shift, oligonucleotide competition, and proteolytic clipping assays. These data suggest that additional proteins are critical for the ability of GATA-3 to activate the TCR beta enhancer. In fibroblasts, the GATA sequence at site TE1 appears to bind a negative regulator. Since this is not true in B cells, B cells and fibroblasts appear to have different mechanisms for negative regulation of the TCR beta enhancer.

scholarly journals GATA elements are necessary for the activity and tissue specificity of the T-cell receptor beta-chain transcriptional enhancer.

1994 ◽  
Vol 14 (6) ◽  
pp. 4286-4294 ◽  
Author(s):  
A J Henderson ◽  
S McDougall ◽  
J Leiden ◽  
K L Calame
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Beta Chain ◽  
Transcriptional Enhancer ◽  
T Cell Receptor Beta ◽  
Beta Enhancer ◽  
Receptor Beta

Three high-affinity binding sites for the GATA family of transcriptional regulators have been identified within the T-cell receptor beta-chain (TCR beta) transcriptional enhancer, and their functional significance has been determined in an effort to understand the T-cell specificity of the enhancer more fully. One site, TE4, is important for activity of the enhancer in T cells. Neither site TE1 nor site TE2 can functionally replace a mutated TE4 site in T cells; however, the same protein, probably GATA-3, binds all three sites, as judged by electrophoretic mobility shift, oligonucleotide competition, and proteolytic clipping assays. These data suggest that additional proteins are critical for the ability of GATA-3 to activate the TCR beta enhancer. In fibroblasts, the GATA sequence at site TE1 appears to bind a negative regulator. Since this is not true in B cells, B cells and fibroblasts appear to have different mechanisms for negative regulation of the TCR beta enhancer.

Unusual immunophenotype of CD8+ T cells in familial hemophagocytic lymphohistiocytosis

Blood ◽  
2004 ◽  
Vol 104 (7) ◽  
pp. 2007-2009 ◽  
Author(s):  
Nitin J. Karandikar ◽  
Steven H. Kroft ◽  
Subramanian Yegappan ◽  
Beverly B. Rogers ◽  
Victor M. Aquino ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Cd8 T Cells ◽  
Hemophagocytic Lymphohistiocytosis ◽  
Cell Receptor ◽  
Lymphoid Cells ◽  
T Cell Subsets ◽  
Familial Hemophagocytic Lymphohistiocytosis ◽  
T Cell Subpopulations

Abstract Familial hemophagocytic lymphohistiocytosis (FHL) is an inherited, fatal disorder of infancy. We report here a 17-day-old female infant who presented with high fever, hepatosplenomegaly, hypertriglyceridemia, hypofibrinogenemia, thrombocytopenia, and liver failure. Leukocytosis was detected with circulating “atypical” lymphoid cells. Flow cytometric studies revealed expanded subpopulations of CD8+ T cells with unusual immunophenotypic features, including a subset that lacked CD5 expression. A liver biopsy showed hemophagocytic lymphohistiocytosis with exuberant infiltrates of CD8+ T cells that lacked perforin. Mutational studies revealed a 666C→A (H222Q) missense mutation in the perforin gene. T-cell receptor studies on flow-sorted T-cell subpopulations revealed no evidence of monoclonality. Analysis of T-cell receptor excision circle levels indicated long proliferative history in the aberrant CD8+ T-cell subsets. This case provides an instructive example of uncontrolled reactive proliferation of CD8+ T cells in FHL, resulting in atypical morphology and unusual immunophenotypic features that might suggest malignancy in other clinical settings.

scholarly journals T-cell leukemias with rearrangement of the gamma but not beta T-cell receptor genes

Blood ◽  
1988 ◽  
Vol 71 (2) ◽  
pp. 356-362 ◽  
Author(s):  
L Foroni ◽  
E Matutes ◽  
J Foldi ◽  
R Morilla ◽  
T Rabbitts ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Lymphoid Cells ◽  
Leukemic Cells ◽  
New Information ◽  
Combined Use ◽  
T Cell Receptor Genes ◽  
Lgl Leukemia

beta and gamma T cell receptor (TCR) gene configuration was studied in 12 patients with large granular lymphocyte T cell leukemia (LGL- leukemia). Both genes were found rearranged in ten cases. In the remaining two patients TCR beta was found in germline configuration. In one of them rearrangement of T cell-rearranging gene gamma (TRG gamma) and a gamma mRNA were demonstrated. We suggest that in this patient the leukemic T cells arose from one of the rare T cells bearing a gamma- delta rather than an alpha-beta TCR heterodimeric molecule. In the other patient several discrete TRG gamma rearrangements were detected. Because her leukemic cells were shown to be monoclonal on the grounds of their karyotype, we suggest that her leukemia originated before any rearrangement had taken place. The combined use of TCR beta and TRG gamma probes provides new information on the origin and clonal expansion of lymphoid cells in LGL-leukemia.

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