HIV-1 Tat modulates T-bet expression and induces Th1 type of immune response

Asavari Kulkarni; Dyavar S. Ravi; Kamini Singh; Shravanti Rampalli; Vrajesh Parekh; Debashis Mitra; Samit Chattopadhyay

doi:10.1016/j.bbrc.2005.02.042

HIV-1 Tat modulates T-bet expression and induces Th1 type of immune response

Asavari Kulkarni, Dyavar S. Ravi, Kamini Singh, Shravanti Rampalli, Vrajesh Parekh, Debashis Mitra, Samit Chattopadhyay

Research output: Contribution to journal › Article › peer-review

8 Scopus citations

Abstract

The HIV-1 transactivator Tat performs various viral and cellular functions. Primarily, it induces processive transcription from the HIV-1 LTR promoter. However, Tat secreted from infected cells is known to activate uninfected lymphocytes through receptors. To further delineate the specific target genes, extracellular Tat was expressed on the cell membrane of stimulator cells and co-cultured with human PBMCs. Along with induced CD4⁺ T cell proliferation and IFN-γ secretion, there was strong upregulation of T-bet expression which is majorly implicated in generating T_H1 type of immune response. To further delineate the effect of extracellular Tat on HIV replication, both p24 analysis and in vivo GFP expression were performed. There was a significant inhibition of HIV-1 replication in human CEM-GFP cell line and hPBMCs. Thus, for the first time we report that apart from its transactivation activity, extracellular Tat acts as a costimulatory molecule that affects viral replication by modulating host immune response through induction of T-bet expression and IFN-γ secretion.

Original language	English (US)
Pages (from-to)	706-712
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	329
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2005.02.042
State	Published - Apr 8 2005
Externally published	Yes

Keywords

HIV-1
HIV-1 replication
IFN-γ
T cell proliferation
T-bet
TCR
Tat

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2005.02.042

Cite this

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title = "HIV-1 Tat modulates T-bet expression and induces Th1 type of immune response",

abstract = "The HIV-1 transactivator Tat performs various viral and cellular functions. Primarily, it induces processive transcription from the HIV-1 LTR promoter. However, Tat secreted from infected cells is known to activate uninfected lymphocytes through receptors. To further delineate the specific target genes, extracellular Tat was expressed on the cell membrane of stimulator cells and co-cultured with human PBMCs. Along with induced CD4+ T cell proliferation and IFN-γ secretion, there was strong upregulation of T-bet expression which is majorly implicated in generating TH1 type of immune response. To further delineate the effect of extracellular Tat on HIV replication, both p24 analysis and in vivo GFP expression were performed. There was a significant inhibition of HIV-1 replication in human CEM-GFP cell line and hPBMCs. Thus, for the first time we report that apart from its transactivation activity, extracellular Tat acts as a costimulatory molecule that affects viral replication by modulating host immune response through induction of T-bet expression and IFN-γ secretion.",

keywords = "HIV-1, HIV-1 replication, IFN-γ, T cell proliferation, T-bet, TCR, Tat",

author = "Asavari Kulkarni and Ravi, {Dyavar S.} and Kamini Singh and Shravanti Rampalli and Vrajesh Parekh and Debashis Mitra and Samit Chattopadhyay",

note = "Funding Information: We would like to thank Dr. G.C. Mishra, Director, NCCS for his constant support to carry out the experiments. We also thank Prof. Thomas August for a kind gift of cDNA expression vector for LAMP-1 and NIH AIDS Reagent Program for CEM-GFP cell line and HIV-1 NL4.3 molecular clone. A. Kulkarni and S. Rampalli were supported by fellowships from CSIR, India. D.S. Ravi and K. Singh were supported by fellowship from UGC and ICMR, India respectively. This work was supported by the Department of Biotechnology (DBT), New Delhi, India.",

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doi = "10.1016/j.bbrc.2005.02.042",

language = "English (US)",

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T1 - HIV-1 Tat modulates T-bet expression and induces Th1 type of immune response

AU - Kulkarni, Asavari

AU - Ravi, Dyavar S.

AU - Singh, Kamini

AU - Rampalli, Shravanti

AU - Parekh, Vrajesh

AU - Mitra, Debashis

AU - Chattopadhyay, Samit

N1 - Funding Information: We would like to thank Dr. G.C. Mishra, Director, NCCS for his constant support to carry out the experiments. We also thank Prof. Thomas August for a kind gift of cDNA expression vector for LAMP-1 and NIH AIDS Reagent Program for CEM-GFP cell line and HIV-1 NL4.3 molecular clone. A. Kulkarni and S. Rampalli were supported by fellowships from CSIR, India. D.S. Ravi and K. Singh were supported by fellowship from UGC and ICMR, India respectively. This work was supported by the Department of Biotechnology (DBT), New Delhi, India.

PY - 2005/4/8

Y1 - 2005/4/8

N2 - The HIV-1 transactivator Tat performs various viral and cellular functions. Primarily, it induces processive transcription from the HIV-1 LTR promoter. However, Tat secreted from infected cells is known to activate uninfected lymphocytes through receptors. To further delineate the specific target genes, extracellular Tat was expressed on the cell membrane of stimulator cells and co-cultured with human PBMCs. Along with induced CD4+ T cell proliferation and IFN-γ secretion, there was strong upregulation of T-bet expression which is majorly implicated in generating TH1 type of immune response. To further delineate the effect of extracellular Tat on HIV replication, both p24 analysis and in vivo GFP expression were performed. There was a significant inhibition of HIV-1 replication in human CEM-GFP cell line and hPBMCs. Thus, for the first time we report that apart from its transactivation activity, extracellular Tat acts as a costimulatory molecule that affects viral replication by modulating host immune response through induction of T-bet expression and IFN-γ secretion.

AB - The HIV-1 transactivator Tat performs various viral and cellular functions. Primarily, it induces processive transcription from the HIV-1 LTR promoter. However, Tat secreted from infected cells is known to activate uninfected lymphocytes through receptors. To further delineate the specific target genes, extracellular Tat was expressed on the cell membrane of stimulator cells and co-cultured with human PBMCs. Along with induced CD4+ T cell proliferation and IFN-γ secretion, there was strong upregulation of T-bet expression which is majorly implicated in generating TH1 type of immune response. To further delineate the effect of extracellular Tat on HIV replication, both p24 analysis and in vivo GFP expression were performed. There was a significant inhibition of HIV-1 replication in human CEM-GFP cell line and hPBMCs. Thus, for the first time we report that apart from its transactivation activity, extracellular Tat acts as a costimulatory molecule that affects viral replication by modulating host immune response through induction of T-bet expression and IFN-γ secretion.

KW - HIV-1

KW - HIV-1 replication

KW - IFN-γ

KW - T cell proliferation

KW - T-bet

KW - TCR

KW - Tat

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ER -

HIV-1 Tat modulates T-bet expression and induces Th1 type of immune response

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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