Human T-cell leukemia virus type 2 induces survival and proliferation of CD34+ TF-1 cells through activation of STAT1 and STAT5 by secretion of interferon-γ and granulocyte macrophage–colony-stimulating factor

Bovolenta, Chiara; Pilotti, Elisabetta; Mauri, Massimiliano; Turci, Marco; Ciancianaini, P.; Fisicaro, Paola; Bertazzoni, Umberto; Poli, Guido; Casoli, Claudio

doi:10.1182/blood.v99.1.224

Cited by 20 publications

(21 citation statements)

References 46 publications

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“…ϩ and CD8 ϩ T cells with HTLV-2 up to 24 h triggers STAT activation is in agreement with our recent observation that incubation of CD34 ϩ TF-1 cells with HTLV-2 induced the secretion of IFN-␥ and GM-CSF, which in turn activated STAT1 and STAT5, respectively (25).…”

Section: Separated Cd4supporting

confidence: 78%

“…In contrast, we recently demonstrated that the ability of the human CD34 ϩ IL-3-dependent TF-1 cell line of proliferating after HTLV-2 exposure in conditions of IL-3 deprivation is the consequence of the production of the GM-CSF and IFN-␥, both signaling through the activation of the Janus kinase (JAK)/STAT pathway (25). In addition, we have recently shown that most (75%) HIV-1 seropositive patients display a constitutive activation of STAT5⌬ and STAT1 in their freshly isolated and unstimulated PBMC (26).…”

Section: H Uman T Cell Leukemia Virus (Htlv)mentioning

confidence: 99%

“…The viral titers of the concentrated virus preparations were defined by levels of p19 Ag in fluids (RETRO-TEK HTLV p19 Ag ELISA; ZeptoMetrix, Buffalo, NY). Cells were incubated with 0.5-1 ng/ml HTLV-2 p19 Gag Ag equivalent for 24 h, as previously described (25,30). PBMC from infected individuals and healthy normal donors were obtained by centrifugation of peripheral venous blood on Ficoll-Hypaque density gradient (Pharmacia Biotech, Uppsala, Sweden) following the standardized procedures.…”

Section: Htlv-2 Strain Pbmc Isolation Cd4mentioning

confidence: 99%

“…WCE were prepared by repeated cycles of cell freezing and thawing as previously described in detail (25). EMSA was performed by incubating WCEs with [␥-…”

Section: Whole-cell Extracts (Wce) and Emsamentioning

confidence: 99%

“…The virions were purified and concentrated as described previously (25,30). The viral titers of the concentrated virus preparations were defined by levels of p19 Ag in fluids (RETRO-TEK HTLV p19 Ag ELISA; ZeptoMetrix, Buffalo, NY).…”

Section: Htlv-2 Strain Pbmc Isolation Cd4mentioning

confidence: 99%

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Retroviral Interference on STAT Activation in Individuals Coinfected with Human T Cell Leukemia Virus Type 2 and HIV-1

Bovolenta¹,

Pilotti

Mauri³

et al. 2002

The Journal of Immunology

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Human T cell leukemia virus (HTLV) type-2 is a human retrovirus whose infection has not been tightly linked to human diseases. However, the fairly high prevalence of this infection among HIV-1-positive individuals indicates the importance of better understanding the potential interference of HTLV-2 infection on HIV-1 infection and AIDS. We previously demonstrated that one signature of PBMC freshly derived from HIV-1-infected individuals is the constitutive activation of a C-terminal truncated STAT5 (STAT5Δ). Therefore, we analyzed the potential activation of STATs in HTLV-2 monoinfected and HTLV-2/HIV-1 dually infected individuals. We observed that PBMC of HTLV-2-infected individuals do not show STAT activation unless they are cultivated ex vivo, in the absence of any mitogenic stimuli, for at least 8 h. The emergence of STAT activation, namely of STAT1, in culture was mostly related to the secretion of IFN-γ. Of note, this phenomenon is not only a characteristic feature of HTLV-2-infected individuals but also occurred with PBMC of HIV-1+ individuals. Surprisingly, HTLV-2/HIV-1 coinfection resulted in low/absent STAT activation in vivo that paralleled a diminished secretion of IFN-γ after ex vivo cultivation. Our findings indicate that both HTLV-2 and HIV-1 infection prime T lymphocytes for STAT1 activation, but they also highlight an interference exerted by HTLV-2 on HIV-1-induced STAT1 activation. Although the nature of such a phenomenon is unclear at the present, these findings support the hypothesis that HTLV-2 may interfere with HIV-1 infection at multiple levels.

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Section: Separated Cd4supporting

confidence: 78%

Section: H Uman T Cell Leukemia Virus (Htlv)mentioning

confidence: 99%

Section: Htlv-2 Strain Pbmc Isolation Cd4mentioning

confidence: 99%

“…WCE were prepared by repeated cycles of cell freezing and thawing as previously described in detail (25). EMSA was performed by incubating WCEs with [␥-…”

Section: Whole-cell Extracts (Wce) and Emsamentioning

confidence: 99%

Section: Htlv-2 Strain Pbmc Isolation Cd4mentioning

confidence: 99%

See 3 more Smart Citations

Retroviral Interference on STAT Activation in Individuals Coinfected with Human T Cell Leukemia Virus Type 2 and HIV-1

Bovolenta¹,

Pilotti

Mauri³

et al. 2002

The Journal of Immunology

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Dexamethasone inhibits camptothecin-induced apoptosis in C6-glioma via activation of Stat5/Bcl-xL pathway

Qian¹,

Xiao²,

Chen³

2009

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Dexamethasone (DX) induces apoptosis resistance in most solid malignant tumors during co-treatment with chemotherapy agents, such as camptothecin (CAM). In this study, we investigated the mechanism by which DX reduces chemotherapy efficiency in C6-glioma. DX reduced CAM-increased DNA fragmentation and caspase-3 activation. The DX’s protection was negated by RU486, an antagonist of glucocorticoid receptor (GR). DX itself increased anti-apoptotic gene, Bcl-xL expression, and its transcription factor, signaling transducer and activator of transcription 5 (Stat5), DNA binding activity and phospho-Stat5 expression. DX blocked the CAM-decreased Bcl-xL and phospho-Stat5 expression, and Stat5 binding activity. RU486 negated DX’s actions. To determine whether Stat5 regulates Bcl-xL expression in CAM -induced cell death, C6-glioma was infected with an adenovirus containing a constitutively activated Stat5-GFP (Ad-Stat5ca). Overexpression of Stat5ca increased Bcl-xL and decreased CAM-induced cell death compared to control adenovirus infected cells; whereas Stat5 siRNA decreased DX-induced Bcl-xL and increased cell death. Phospho-Stat5 expression was observed in the nuclear extract by co-immunoprecipitation with an anti-GR antibody, indicating that Stat5 and GR were interactive and formed a complex in the nuclei. These results suggest that DX’s prevention from CAM -induced apoptosis and RU486’s antagonism of DX’s protection may be through Stat5/Bcl-xL signal pathway regulated by a GR.

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Single-cell RNA sequencing unveils the communications between malignant T and myeloid cells contributing to tumor growth and immunosuppression in cutaneous T-cell lymphoma

Cai

et al. 2022

Cancer Letters

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Human T-cell leukemia virus type 2 induces survival and proliferation of CD34+ TF-1 cells through activation of STAT1 and STAT5 by secretion of interferon-γ and granulocyte macrophage–colony-stimulating factor

Cited by 20 publications

References 46 publications

Retroviral Interference on STAT Activation in Individuals Coinfected with Human T Cell Leukemia Virus Type 2 and HIV-1

Retroviral Interference on STAT Activation in Individuals Coinfected with Human T Cell Leukemia Virus Type 2 and HIV-1

Dexamethasone inhibits camptothecin-induced apoptosis in C6-glioma via activation of Stat5/Bcl-xL pathway

Single-cell RNA sequencing unveils the communications between malignant T and myeloid cells contributing to tumor growth and immunosuppression in cutaneous T-cell lymphoma

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