scholarly journals Single-cell cloning of human T-cell lines reveals clonal variation in cell death responses to chemotherapeutics

2019 ◽  
Vol 237 ◽  
pp. 69-77 ◽  
Author(s):  
Kathleen Hanlon ◽  
Alex Thompson ◽  
Lorena Pantano ◽  
John N. Hutchinson ◽  
Arshed Al-Obeidi ◽  
...  
1992 ◽  
Vol 66 (11) ◽  
pp. 6788-6793 ◽  
Author(s):  
D Ou ◽  
P Chong ◽  
Y Choi ◽  
P McVeigh ◽  
W A Jefferies ◽  
...  

1997 ◽  
pp. 105-117 ◽  
Author(s):  
Edoardo Alesse ◽  
Luisa Di Marzio ◽  
Paola Roncaioli ◽  
Francesca Zazzeroni ◽  
Adriano Angelucci ◽  
...  

Blood ◽  
2003 ◽  
Vol 102 (12) ◽  
pp. 4130-4136 ◽  
Author(s):  
Hye-Kyung Chung ◽  
Howard A. Young ◽  
Peter K. C. Goon ◽  
Gisela Heidecker ◽  
Gerald L. Princler ◽  
...  

Abstract Human T-cell leukemia virus type 1 (HTLV-1) infection profoundly alters T-cell gene expression, and the dysregulated synthesis of cytokines could influence the course and pathologic consequences of infection. In the process of screening T-cell lines for T helper 1 (Th1) and Th2 cytokine mRNAs, we observed that interleukin-13 (IL-13) mRNA was highly expressed in HTLV-1-infected, IL-2-dependent T-cell lines. IL-9 and interferon gamma (IFN-γ) mRNAs were also expressed at high levels in chronically infected cell lines. IL-5 mRNA was detected in 60% of the HTLV-1-infected cell lines, but mRNAs for IL-4, IL-10, IL-2, and IL-15 were either below detection limits or did not correlate with HTLV-1 infection. Transcriptional activation of the IL-13 promoter by the HTLV-1 Tax trans-regulatory protein was demonstrated in Jurkat T cells transiently transfected with an IL-13 promoter-reporter plasmid. The clinical relevance of these observations was demonstrated by immunofluorescent staining and flow cytometry of lymphocytes obtained from HTLV-1-infected patients. These studies revealed that IL-13 production was directly related to the level of Tax expression in the infected CD4+ T cells soon after in vitro culture. As IL-13 plays key roles in tumor immunosurveillance, asthma, and central nervous system inflammation, it may contribute to the pathophysiology of HTLV-1-associated diseases. (Blood. 2003;102:4130-4136)


1996 ◽  
Vol 97 (1) ◽  
pp. 410-410
Author(s):  
M HERMANOFF ◽  
G KHARE ◽  
S TILLES ◽  
L ROSENWASSER

Author(s):  
S. Dube ◽  
B. Paul ◽  
V. Bryz-Gornia ◽  
C. Stephens ◽  
S. Erensoy ◽  
...  

Blood ◽  
1997 ◽  
Vol 90 (5) ◽  
pp. 1893-1901 ◽  
Author(s):  
David E. Joyce ◽  
Yan Chen ◽  
Rochelle A. Erger ◽  
Gary A. Koretzky ◽  
Steven R. Lentz

Abstract The proteolytically activated thrombin receptor (TR) is expressed by T lymphocytes, which suggests that thrombin may modulate T-cell activation at sites of hemostatic stress. We examined the relationship between TR function and T-cell activation in the Jurkat human T-cell line and in T-cell lines with defined defects in T-cell antigen receptor (TCR) function. Stimulation with thrombin or the synthetic TR peptide SFLLRN produced intracellular Ca2+ transients in Jurkat cells. As the concentration of TR agonist was increased, peak Ca2+ mobilization increased, but influx of extracellular Ca2+ decreased. TR signaling was enhanced in a TCR-negative Jurkat line and in T-cell lines deficient in the tyrosine kinase lck or the tyrosine phosphatase CD45, both of which are essential for normal TCR function. TCR cross-linking with anti-CD3 IgM desensitized TR signaling in Jurkat cells, but not in CD45-deficient cells. A proteinase-activated receptor (PAR-2)–specific agonist peptide, SLIGKV, produced small Ca2+ transients in both MEG-01 human megakaryocytic cells and Jurkat cells, but was less potent than the TR-specific agonist TFRIFD in both cell types. Like TR signaling, PAR-2 signaling was enhanced in TCR-negative or lck-deficient Jurkat clones. These findings provide evidence for functional cross-talk between proteolytically activated receptors and the TCR.


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