scholarly journals Infection with human T-lymphotropic viruses leads to constitutive expression of leukemia inhibitory factor and interleukin-6

Blood ◽  
1993 ◽  
Vol 81 (7) ◽  
pp. 1827-1832 ◽  
Author(s):  
RB Lal ◽  
D Rudolph ◽  
C Buckner ◽  
D Pardi ◽  
WC Hooper
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Interleukin 6 ◽  
Leukemia Inhibitory Factor ◽  
Constitutive Expression ◽  
Cellular Systems ◽  
Inhibitory Factor ◽  
Infected Cell Line ◽  
Proliferating Cells ◽  
Human T Cell

Abstract Leukemia inhibitory factor (LIF), similar to interleukin-6 (IL-6), is a glycoprotein growth factor and differentiation regulator that has pleiotropic activity in several cellular systems. Recent reports of constitutive IL-6 production from spontaneously proliferating cells from human T-cell leukemia virus (HTLV)-infected individuals led us to examine the expression of IL-6 and LIF during HTLV infection. In vitro infection of peripheral blood lymphocytes with HTLV-I was associated with production of both soluble LIF and IL-6 in conjunction with the increasing HTLV antigen concentration. Northern blot analysis of T-cell lines generated from individuals infected with HTLV-I (MT-2, HuT-102, FS, EG, SP) and HTLV-II (Mo-T, H2A, H2E) demonstrated a marked increase in constitutive expression of LIF and IL-6 transcripts, as compared with uninfected cell lines (HuT-78, Jurkat). The constitutive expression of LIF and IL-6 was independent of presence of IL-2 in the culture medium, as both IL-2-independent (MT-2, HuT-102, SP, Mo-T) and IL-2-dependent (FS, EG, H2A, H2E) cell lines expressed LIF and IL-6 transcripts. Furthermore, LIF and IL-6 RNA expression in an HTLV-I- infected cell line (MT-2) was enhanced by phorbol ester stimulation via mechanisms that appear to be dependent on the posttranscriptional regulatory controls. These results show that both LIF and IL-6 are produced by HTLV-I- and HTLV-II-infected cells, which could potentially alter the transcriptional regulation of HTLV gene expression by inducing certain early response genes.

scholarly journals Infection with human T-lymphotropic viruses leads to constitutive expression of leukemia inhibitory factor and interleukin-6

Blood ◽  
1993 ◽  
Vol 81 (7) ◽  
pp. 1827-1832
Author(s):  
RB Lal ◽  
D Rudolph ◽  
C Buckner ◽  
D Pardi ◽  
WC Hooper
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Interleukin 6 ◽  
Leukemia Inhibitory Factor ◽  
Constitutive Expression ◽  
Cellular Systems ◽  
Inhibitory Factor ◽  
Infected Cell Line ◽  
Proliferating Cells ◽  
Human T Cell

Leukemia inhibitory factor (LIF), similar to interleukin-6 (IL-6), is a glycoprotein growth factor and differentiation regulator that has pleiotropic activity in several cellular systems. Recent reports of constitutive IL-6 production from spontaneously proliferating cells from human T-cell leukemia virus (HTLV)-infected individuals led us to examine the expression of IL-6 and LIF during HTLV infection. In vitro infection of peripheral blood lymphocytes with HTLV-I was associated with production of both soluble LIF and IL-6 in conjunction with the increasing HTLV antigen concentration. Northern blot analysis of T-cell lines generated from individuals infected with HTLV-I (MT-2, HuT-102, FS, EG, SP) and HTLV-II (Mo-T, H2A, H2E) demonstrated a marked increase in constitutive expression of LIF and IL-6 transcripts, as compared with uninfected cell lines (HuT-78, Jurkat). The constitutive expression of LIF and IL-6 was independent of presence of IL-2 in the culture medium, as both IL-2-independent (MT-2, HuT-102, SP, Mo-T) and IL-2-dependent (FS, EG, H2A, H2E) cell lines expressed LIF and IL-6 transcripts. Furthermore, LIF and IL-6 RNA expression in an HTLV-I- infected cell line (MT-2) was enhanced by phorbol ester stimulation via mechanisms that appear to be dependent on the posttranscriptional regulatory controls. These results show that both LIF and IL-6 are produced by HTLV-I- and HTLV-II-infected cells, which could potentially alter the transcriptional regulation of HTLV gene expression by inducing certain early response genes.

scholarly journals Rat lymphoid cell lines producing human T cell leukemia virus. II. Constitutive expression of rat interleukin 2 receptor.

1985 ◽  
Vol 161 (5) ◽  
pp. 924-934 ◽  
Author(s):  
J Yodoi ◽  
M Okada ◽  
Y Tagaya ◽  
K Teshigawara ◽  
K Fukui ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Lymphoid Cell ◽  
Interleukin 2 ◽  
Constitutive Expression ◽  
Receptor Expression ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Human T Cell ◽  
Lymphoid Cell Lines

Three rat lymphoid cell lines (TARS-1, TARL-2, and TART-1) (12) transformed by human T cell leukemia/lymphoma virus I (HTLV-I) had rearrangement of the beta chain gene of the T cell antigen receptor, and had integrated proviral DNA from HTLV-I in their genomes. As is the case with adult T cell leukemia (ATL)-derived human T cell lines transformed by HTLV-I, these rat cell lines unequivocally expressed interleukin 2 (IL-2) receptor, as determined by radiolabeled IL-2 binding. By Scatchard plot analysis, one of the cell lines, TART-1, proved to have high affinity receptors (Ka = 1.3 X 10(11)/M and 8.8 X 10(9)/M). Rat IL-2 receptor, not human IL-2 receptor, was expressed on HTLV+ rat cell lines, as demonstrated by the fact that they expressed antigens reactive with monoclonal antibodies (ART-18) against rat IL-2 receptor, but not with anti-Tac antibodies. The collective evidence indicates that the endogenous IL-2 receptor gene is activated in human and rat lymphoid cell lines with HTLV-I production. The mechanism of abnormal IL-2 receptor expression in HTLV infection is discussed.

scholarly journals Ciliary neurotropic factor, interleukin 11, leukemia inhibitory factor, and oncostatin M are growth factors for human myeloma cell lines using the interleukin 6 signal transducer gp130.

1994 ◽  
Vol 179 (4) ◽  
pp. 1337-1342 ◽  
Author(s):  
X G Zhang ◽  
J J Gu ◽  
Z Y Lu ◽  
K Yasukawa ◽  
G D Yancopoulos ◽  
...  
Keyword(s):  
Cell Lines ◽  
Interleukin 6 ◽  
Leukemia Inhibitory Factor ◽  
Biological Activities ◽  
Myeloma Cell ◽  
Oncostatin M ◽  
Inhibitory Factor ◽  
Signal Transducer ◽  
Neurotropic Factor ◽  
Human Myeloma Cell

Interleukin 6 (IL-6) is a major growth factor for tumor plasma cells involved in human multiple myeloma (MM). In particular, human myeloma cell lines (HMCL), whose growth is completely dependent on addition of exogenous IL-6, can be obtained reproducibly from every patient with terminal disease. Four cytokines, ciliary neurotropic factor (CNTF), IL-11, leukemia inhibitory factor (LIF), and oncostatin M (OM), use the same transducer chain (signal transducer gp130) as IL-6 and share numerous biological activities with this IL. We found that these four cytokines stimulated proliferation and supported the long-term growth of two out of four IL-6-dependent HMCL obtained in our laboratory. Half-maximal proliferation was obtained with cytokine concentrations ranging from 0.4 to 1.2 ng/ml for IL-11, LIF, and OM. CNTF worked at high concentrations only (90 ng/ml), but addition of soluble CNTF receptor increased sensitivity to CNTF 30-fold. The growth-promoting effect of these four cytokines was abrogated by anti-gp130 antibodies, contrary to results for anti-IL-6 receptor or anti-IL-6 antibodies. No detectable changes in the morphology and phenotype were found when myeloma cells were cultured with one of these four cytokines instead of IL-6. Concordant with their IL-6-dependent growth, the four HMCL expressed membrane IL-6R and gp130 detected by FACS analysis. LIF-binding chain gene (LIFR) was expressed only in the two HMCL responsive to LIF and OM.

scholarly journals Constitutive expression of the cyclooxygenase-2 gene in T-cell lines infected with human T cell leukemia virus type I

2001 ◽  
Vol 94 (6) ◽  
pp. 813-819 ◽  
Author(s):  
Naoki Mori ◽  
Hiroyasu Inoue ◽  
Tsutomu Yoshida ◽  
Tadashi Tanabe ◽  
Naoki Yamamoto
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Leukemia Virus ◽  
Constitutive Expression ◽  
Type I ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
T Cell Lines

Identification of T-cell epitopes on E2 protein of rubella virus, as recognized by human T-cell lines and clones.

1992 ◽  
Vol 66 (11) ◽  
pp. 6788-6793 ◽  
Author(s):  
D Ou ◽  
P Chong ◽  
Y Choi ◽  
P McVeigh ◽  
W A Jefferies ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Rubella Virus ◽  
T Cell Epitopes ◽  
E2 Protein ◽  
Human T Cell ◽  
T Cell Lines

Structure of the two promoters of the human lck gene: differential accumulation of two classes of lck transcripts in T cells

1989 ◽  
Vol 9 (5) ◽  
pp. 2173-2180
Author(s):  
T Takadera ◽  
S Leung ◽  
A Gernone ◽  
Y Koga ◽  
Y Takihara ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Human Peripheral Blood ◽  
Specific Gene ◽  
Type I ◽  
Type Ii ◽  
Carcinoma Cell Lines ◽  
Human T Cell

The human T-cell- or lymphocyte-specific gene, lck, encodes a tyrosine kinase and is a member of the src family. In this report we demonstrate that there are two classes of human lck transcripts (types I and II), containing different 5'-untranslated regions, which are expressed from two distinct promoters. No apparent sequence similarity was observed between the 5'-flanking regions of the two promoters. The expression of lck in human T-cell leukemia and carcinoma cell lines and in human peripheral blood T lymphocytes was examined by S1 nuclease and primer extension mapping and by Northern (RNA) blot analysis of total cellular RNA. The following results were obtained. (i) Two RNA start sites in the downstream promoter were used to generate type I transcripts. (ii) The major human type I start site has not been described for the mouse. (iii) At least five RNA start sites in the upstream promoter were used to generate type II transcripts. (iv) In T cells and in two colon carcinoma cell lines, type II transcripts were present in higher amounts than type I transcripts. (v) In T cells treated with phytohemagglutinin, tetradecanoylphorbol acetate, and cyclosporin A, the modulation of lck expression was associated primarily with changes in levels of type II transcripts. The above results suggest that the two human lck promoters are utilized differentially and may be regulated independently during certain physiological states.

scholarly journals Synthetic (E)-3-Phenyl-5-(phenylamino)-2-styryl-1,3,4-thiadiazol-3-ium Chloride Derivatives as Promising Chemotherapy Agents on Cell Lines Infected with HTLV-1

Molecules ◽  
2020 ◽  
Vol 25 (11) ◽  
pp. 2537
Author(s):  
Danilo Sousa-Pereira ◽  
Thais Silva de Oliveira ◽  
Rojane O. Paiva ◽  
Otávio Augusto Chaves ◽  
José C. Netto-Ferreira ◽  
...  
Keyword(s):  
Molecular Docking ◽  
T Cell ◽  
Cell Lines ◽  
Pharmacokinetic Profile ◽  
Biological Evaluation ◽  
Spectroscopic Techniques ◽  
Time Resolved ◽  
Adult T Cell Leukemia ◽  
Human T Cell ◽  
Ic50 Values

Synthesis of four compounds belonging to mesoionic class, (E)-3-phenyl-5-(phenylamino)-2-styryl-1,3,4-thiadiazol-3-ium chloride derivatives (5a–d) and their biological evaluation against MT2 and C92 cell lines infected with human T-cell lymphotropic virus type-1 (HTLV-1), which causes adult T-cell leukemia/lymphoma (ATLL), and non-infected cell lines (Jurkat) are reported. The compounds were obtained by convergent synthesis under microwave irradiation and the cytotoxicity was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Results showed IC50 values of all compounds in the range of 1.51–7.70 μM in HTLV-1-infected and non-infected cells. Furthermore, it was observed that 5b could induce necrosis after 24 h for Jurkat and MT2 cell lines. The experimental (fluorimetric method) and theoretical (molecular docking) results suggested that the mechanism of action for 5b could be related to its capacity to intercalate into DNA. Moreover, the preliminary pharmacokinetic profile of the studied compounds (5a–d) was obtained through human serum albumin (HSA) binding affinity using multiple spectroscopic techniques (circular dichroism, steady-state and time-resolved fluorescence), zeta potential and molecular docking calculations. The interaction HSA:5a–d is spontaneous and moderate (Ka ~ 104 M−1) via a ground-state association, without significantly perturbing both the secondary and surface structures of the albumin in the subdomain IIA (site I), indicating feasible biodistribution in the human bloodstream.

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