scholarly journals Myb binding sites mediate negative regulation of c-myb expression in T- cell lines

Blood ◽  
1995 ◽  
Vol 86 (5) ◽  
pp. 1873-1880 ◽  
Author(s):  
J Guerra ◽  
DA Withers ◽  
LM Boxer
Keyword(s):  
T Cell ◽  
Binding Site ◽  
Cell Line ◽  
Cell Lines ◽  
Binding Sites ◽  
Myeloid Cell ◽  
Hematopoietic Cell ◽  
Wild Type ◽  
Myeloid Cell Line ◽  
T Cell Lines

In hematopoietic cell development, the c-myb transcription factor plays an important role. c-myb mRNA is expressed at high levels in immature proliferating cells and in leukemic cells. We have investigated the regulatory role of Myb protein binding to the human c-myb promoter. Three Myb binding sites have been described at approximately 600 bp upstream of the cap site. By transient transfection assays in hematopoietic cell lines, we found that deletion of the previously defined most 52 Myb binding site had no effect on activity, whereas deletion of the region containing the remaining two Myb binding sites resulted in an increase in activity in both a T-cell line and a myeloid cell line. To specifically test the importance of these two Myb binding sites, the activity of three-point mutation constructs was measured. Mutation of either Myb binding site resulted in an increase in activity compared with the wild-type promoter in T cells. Mutation of both sites produced even higher activity. Transfection of the Myb site mutants into the myeloid cell line resulted in no change in activity compared with the wild type construct. Results from gel shift analysis, UV cross- linking, and Western blots showed that both c-Myb and B-Myb bound to the Myb I and II sites. We conclude that the Myb family proteins negatively regulate c-myb expression in T-cell lines in contrast to the positive regulation via these sites, which has been shown in fibroblasts. In addition, in a myeloid cell line, the Myb binding sites are nonfunctional.

scholarly journals Interleukin 2 induces antigen-reactive T cell lines to secrete BCGF-I.

1983 ◽  
Vol 158 (6) ◽  
pp. 2024-2039 ◽  
Author(s):  
M Howard ◽  
L Matis ◽  
T R Malek ◽  
E Shevach ◽  
W Kell ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Interleukin 2 ◽  
Activated T Lymphocytes ◽  
T Cell Lines ◽  
Activated B Cells

Antigen-activated T lymphocytes produce within 24 h of stimulation a factor that is indistinguishable biochemically and functionally from the B cell co-stimulating growth factor, BCGF-I, originally identified in induced EL4 supernatants: Supernatants from antigen-stimulated T cell lines are not directly mitogenic for resting B cells, but synergize in an H-2-unrestricted manner with anti-Ig activated B cells to produce polyclonal proliferation but not antibody-forming-cell development; biochemical studies reveal the B cell co-stimulating factor present in antigen-stimulated T cell line supernatants is identical by phenyl Sepharose chromatography and isoelectric focusing (IEF) to EL4 supernatant BCGF-I. We thus conclude that normal T cells produce BCGF-I in response to antigenic stimulation. Analysis of the mechanism of BCGF-I production by antigen-stimulated T cells showed that optimum amounts of BCGF-I were obtained as quickly as 24 h post-stimulation, and that the factor producing cells in the T cell line investigated bore the Lyt-1+2- phenotype. As few as 10(4) T cells produced sufficient BCGF-I to support the proliferation of 5 X 10(4) purified anti-Ig activated B cells. Finally, the activation of normal T cell lines to produce BCGF-I required either antigen presented in the context of syngeneic antigen-presenting cells (APC) or interleukin 2 (IL-2).

The Leukemic Myeloid Cell Line OMA-AML-1: AnIn VitroModel of Hematopoietic Cell Differentiation

1994 ◽  
Vol 13 (1-2) ◽  
pp. 169-178 ◽  
Author(s):  
Samuel J. Pirruccello ◽  
John D. Jackson ◽  
J. Graham Sharp
Keyword(s):  
Cell Differentiation ◽  
Cell Line ◽  
Myeloid Cell ◽  
Hematopoietic Cell ◽  
Myeloid Cell Line

scholarly journals Identification of an env-defective HIV-1 mutant capable of spontaneous reversion to a wild-type phenotype in certain T-cell lines

2014 ◽  
Vol 11 (1) ◽  
pp. 177 ◽  
Author(s):  
Yudong Quan ◽  
Hongtao Xu ◽  
Victor G Kramer ◽  
Yingshan Han ◽  
Richard D Sloan ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Wild Type ◽  
Spontaneous Reversion ◽  
Wild Type Phenotype ◽  
T Cell Lines ◽  
Hiv 1

scholarly journals Establishment of T cell lines to bovine beta-casein and beta-casein-derived epitopes in patients with type 1 diabetes

2003 ◽  
Vol 176 (1) ◽  
pp. 143-150 ◽  
Author(s):  
L Monetini ◽  
F Barone ◽  
L Stefanini ◽  
A Petrone ◽  
T Walk ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
T Cell ◽  
Beta Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Diabetic Patients ◽  
Beta Casein ◽  
T Cell Lines ◽  
Human Insulinoma

Enhanced cellular immune response to bovine beta-casein has been reported in patients with type 1 diabetes. In this study we aimed to establish beta-casein-specific T cell lines from newly diagnosed type 1 diabetic patients and to characterise these cell lines in terms of phenotype and epitope specificity. Furthermore, since sequence homologies exist between beta-casein and putative beta-cell autoantigens, reactivity to the latter was also investigated. T cell lines were generated from the peripheral blood of nine recent onset type 1 diabetic patients with different HLA-DQ and -DR genotypes, after stimulation with antigen pulsed autologous irradiated antigen presenting cells (APCs) and recombinant human interleukin-2 (rhIL-2). T cell line reactivity was evaluated in response to bovine beta-casein, to 18 overlapping peptides encompassing the whole sequence of beta-casein and to beta-cell antigens, including the human insulinoma cell line, CM, and a peptide from the beta-cell glucose transporter, GLUT-2. T cell lines specific to beta-casein could not be isolated from HLA-matched and -unmatched control subjects. beta-Casein T cell lines reacted to different sequences of the protein, however a higher frequency of T cell reactivity was observed towards the C-terminal portion (peptides B05-14, and B05-17 in 5/9 and 4/9 T cell lines respectively). Furthermore, we found that 1 out of 9 beta-casein-specific T cell lines reacted also to the homologous peptide from GLUT-2, and that 3 out of 4 of tested cell lines reacted also to extracts of the human insulinoma cell line, CM. We conclude that T cell lines specific to bovine beta-casein can be isolated from the peripheral blood of patients with type 1 diabetes; these cell lines react with multiple and different sequences of the protein particularly towards the C-terminal portion. In addition, reactivity of beta-casein T cell lines to human insulinoma extracts and GLUT-2 peptide was detected, suggesting that the potential cross-reactivity with beta-cell antigens deserves further investigation.

scholarly journals T cell growth factor receptors. Quantitation, specificity, and biological relevance

1981 ◽  
Vol 154 (5) ◽  
pp. 1455-1474 ◽  
Author(s):  
RJ Robb ◽  
A Munck ◽  
KA Smith
Keyword(s):  
T Cells ◽  
T Cell ◽  
Growth Factor ◽  
Cell Lines ◽  
Binding Sites ◽  
Activated T Cells ◽  
Receptor Sites ◽  
Polypeptide Hormones ◽  
T Cell Lines ◽  
T Cell Growth Factor

To examine directly the hypothesis that T cell growth factor (TCGF) interacts with target cells in a fashion similar to polypeptide hormones, the binding of radiolabeled TCGF to various cell populations was investigated. The results indicate that TCGF interacts with activated T cells via a receptor through which it initiates the T cell proliferative response. Internally radiolabeled TCGF, prepared from a human T leukemia cell line and purified by gel filtration and isoelectric focusing, retained biological activity and was uniform with respect to size and charge. Binding of radiolabeled TCGF to TCGF-dependent cytolytic T cells occurred rapidly (within 15 rain at 37 degrees C) and was both saturable and largely reversible. In addition, at 37 degrees C, a receptor- and lysosome-dependent degradation of TCGF occurred. Radiolabeled TCGF binding was specific for activated, TCGF-responsive T cells. Whereas unstimulated lymphocytes of human or murine origin and lipopolysaccharide-activated B cell blasts expressed few if any detectable binding sites, lectin- or alloantigen-activated cells had easily detectable binding sites. Moreover, compared with lectin- or alloantigen-activated T cells, long-term TCGF-dependent cytolytic and helper T cell lines and TCGF-dependent neo-plastic T cell lines bound TCGF with a similar affinity (dissociation constant of 5-25 pM) and expressed a similar number of receptor sites per cell (5,000-15,000). In contrast, a number of TCGF-independent cell lines of T cell, B cell, or myeloid origin did not bind detectable quantities of radiolabeled TCGF. Binding of radiolabeled TCGF to TCGF-responsive cells was specific, in that among several growth factors and polypeptide hormones tested, only TCGF competed for binding. Finally, the relative magnitude of T cell proliferation induced by a given concentration of TCGF closely paralleled the fraction of occupied receptor sites. As the extent of T cell clonal expansion depends on TCGF and on the TCGF receptor, the dissection of the molecular events surrounding the interaction of TCGF and its receptor that these studies permit, should provide new insight into the hormonelike regulation of the immune response by this lymphokine.

scholarly journals A Macrophage Differentiating Factor Derived from Human T Cell Line HUT102 Acting on a Mouse Myeloid Cell Line M1.

1993 ◽  
Vol 171 (1) ◽  
pp. 43-52
Author(s):  
HIROYUKI KANNO ◽  
MASATO NOSE ◽  
TAMOTSU NIKI ◽  
MASAAKI MIYAZAWA ◽  
MASAHISA KYOGOKU
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Myeloid Cell ◽  
Human T Cell ◽  
Myeloid Cell Line ◽  
Human T Cell Line

Human Helper T Cell Lines Established by Coculture of Normal Human Cord Leukocytes with an HTLV-Il-infected Rabbit Leukocyte Cell Line (Ra-IIA)

2008 ◽  
Vol 42 (5) ◽  
pp. 347-352
Author(s):  
Kazuhiko Hayashi ◽  
Nobuya Ohara ◽  
Kotaro Fujiwara ◽  
Hiroyuki Aoki ◽  
Kiyoshi Takahashi ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Helper T Cell ◽  
Infected Rabbit ◽  
Normal Human ◽  
T Cell Lines

scholarly journals Immunoregulation of cutaneous leishmaniasis. T cell lines that transfer protective immunity or exacerbation belong to different T helper subsets and respond to distinct parasite antigens.

1988 ◽  
Vol 168 (5) ◽  
pp. 1675-1684 ◽  
Author(s):  
P Scott ◽  
P Natovitz ◽  
R L Coffman ◽  
E Pearce ◽  
A Sher
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Leishmania Major ◽  
Active Immunization ◽  
Th2 Cells ◽  
Antigen Specificity ◽  
T Helper Subsets ◽  
T Cell Lines ◽  
Th1 And Th2

BALB/c mice can be protected against a normally fatal Leishmania major infection by immunization with a partially purified, soluble subfraction of the parasite (fraction 9). In this study, we demonstrate that a T cell line established against fraction 9, designated line 9, transfers protection equivalent to that obtained by active immunization. In contrast, T cell lines (lines 1 and 9.2) responsive to a nonprotective soluble fraction (fraction 1) not only failed to protect BALB/c mice against L. major, but exacerbated the infection. Most importantly, in addition to differing in their antigen specificity, protective and exacerbative T cells lines could be distinguished on the basis of the lymphokines produced, a characteristic previously used to separate murine Th cells into two subsets, designated Th1 and Th2. We found that the protective cell line, line 9, displayed the Th1 property of secreting IL-2 and IFN-gamma, while the exacerbating lines secreted IL-4 and IL-5, a characteristic of Th2 cells. Our results demonstrate that Th1 and Th2 cells may have dramatically different effects on the outcome of an infection, and suggest that susceptibility and resistance in experimental leishmaniasis may depend upon a balance between the Th subsets induced.

scholarly journals The human OX40/gp34 system directly mediates adhesion of activated T cells to vascular endothelial cells.

1996 ◽  
Vol 183 (5) ◽  
pp. 2185-2195 ◽  
Author(s):  
A Imura ◽  
T Hori ◽  
K Imada ◽  
T Ishikawa ◽  
Y Tanaka ◽  
...  
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
T Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Cell Leukemia ◽  
Activated T Cells ◽  
T Cell Lines

Fresh leukemic cells from patients with adult T cell leukemia (ATL) and some ATL-derived T cell lines show adhesion to human umbilical vein endothelial cells (HUVECs) mainly through E-selectin, but a proportion of this binding remains unaffected by the addition of combinations of antibodies against known adhesion molecules. By immunizing mice with one of such cell lines, we established monoclonal antibodies (mAbs), termed 131 and 315, that recognize a single cell surface antigen (Ag) and inhibit the remaining pathway of the adhesion. These mAbs did not react with normal resting peripheral blood mononuclear cells (PBMC) or most of the cell lines tested except for two other human T cell leukemia virus type I (HTLV-I)-infected T cell lines. After stimulation with phytohemagglutinin (PHA), PBMC expressed Ag 131/315 transiently, indicating that these mAbs define a T cell activation Ag. Western blotting and immunoprecipitation revealed that Ag 131/315 has an apparent molecular mass of 50 kD. Expression cloning was done by transient expression in COS-7 cells and immunological selection to isolate a cDNA clone encoding Ag 131/315. Sequence analysis of the cDNA indicated that it is identical to human OX40, a member of the tumor necrosis factor/nerve growth factor receptor family. We then found that gp34, the ligand of OX40, was expressed on HUVECs and other types of vascular endothelial cells. Furthermore, it was shown that the adhesion of CD4+ cells of PHA-stimulated PBMC to unstimulated HUVECs was considerably inhibited by either 131 or 315. Finally, OX40 transfectants of Kit 225, a human interleukin 2-dependent T cell line, were bound specifically to gp34 transfectants of MMCE, a mouse epithelial cell line, and this binding was blocked by either 315 or 5A8, an anti-gp34 mAb. These results indicate that the OX40/gp34 system directly mediates adhesion of activated T cells or OX40+-transformed T cells to vascular endothelial cells.

Non-MHC-restricted target-cell lysis by a CD4−CD− TCRαβ T-cell line, as well as by TCR4gMδ T-cell lines, results from lymphokine-activated killing

2007 ◽  
Vol 48 (1) ◽  
pp. 142-147 ◽  
Author(s):  
Richard T. Maziarz ◽  
Veronika Groh ◽  
Margaret Prendergast ◽  
Marina Fabbi ◽  
Jack L. Strominger ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Target Cell ◽  
Cell Lysis ◽  
T Cell Lines
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