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The MHC-II transactivator CIITA inhibits Tat function and HIV-1 replication in human myeloid cells

Overview of attention for article published in Journal of Translational Medicine, April 2016
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  • Above-average Attention Score compared to outputs of the same age (58th percentile)
  • Above-average Attention Score compared to outputs of the same age and source (57th percentile)

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2 tweeters

Citations

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11 Dimensions

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Title
The MHC-II transactivator CIITA inhibits Tat function and HIV-1 replication in human myeloid cells
Published in
Journal of Translational Medicine, April 2016
DOI 10.1186/s12967-016-0853-5
Pubmed ID
Authors

Greta Forlani, Filippo Turrini, Silvia Ghezzi, Alessandra Tedeschi, Guido Poli, Roberto S. Accolla, Giovanna Tosi

Abstract

We previously demonstrated that the HLA class II transactivator CIITA inhibits HIV-1 replication in T cells by competing with the viral transactivator Tat for the binding to Cyclin T1 subunit of the P-TEFb complex. Here, we analyzed the anti-viral function of CIITA in myeloid cells, another relevant HIV-1 target cell type. We sinvestigated clones of the U937 promonocytic cell line, either permissive (Plus) or non-permissive (Minus) to HIV-1 replication. This different phenotype has been associated with the expression of TRIM22 in U937 Minus but not in Plus cells. U937 Plus cells stably expressing CIITA were generated and HLA-II positive clones were selected by cell sorting and cloning. HLA and CIITA proteins were analyzed by cytofluorometry and western blotting, respectively. HLA-II DR and CIITA mRNAs were quantified by qRT-PCR. Tat-dependent transactivation was assessed by performing the HIV-1 LTR luciferase gene reporter assay. Cells were infected with HIV-1 and viral replication was evaluated by measuring the RT activity in culture supernatants. CIITA was expressed only in HLA-II-positive U937 Minus cells, and this was strictly correlated with inhibition of Tat-dependent HIV-1 LTR transactivation in Minus but not in Plus cells. Overexpression of CIITA in Plus cells restored the suppression of Tat transactivation, confirming the inhibitory role of CIITA. Importantly, HIV-1 replication was significantly reduced in Plus-CIITA cells with respect to Plus parental cells. This effect was independent of TRIM22 as CIITA did not induce TRIM22 expression in Plus-CIITA cells. U937 Plus and Minus cells represent an interesting model to study the role of CIITA in HIV-1 restriction in the monocytic/macrophage cell lineage. The differential expression of CIITA in CIITA-negative Plus and CIITA-positive Minus cells correlated with their capacity to support or not HIV-1 replication, respectively. In Minus cells CIITA targeted the viral transactivator Tat to inhibit HIV-1 replication. The generation of Plus-CIITA cells was instrumental to demonstrate the specific contribution of CIITA in terms of inhibition of Tat activity and HIV-1 restriction, independently from other cellular factors, including TRIM22. Thus, CIITA acts as a general restriction factor against HIV-1 not only in T cells but also in myeloid cells.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 16 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 16 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 4 25%
Student > Postgraduate 3 19%
Student > Ph. D. Student 2 13%
Student > Bachelor 2 13%
Researcher 2 13%
Other 2 13%
Unknown 1 6%
Readers by discipline Count As %
Immunology and Microbiology 7 44%
Agricultural and Biological Sciences 4 25%
Biochemistry, Genetics and Molecular Biology 2 13%
Psychology 1 6%
Neuroscience 1 6%
Other 0 0%
Unknown 1 6%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 21 April 2016.
All research outputs
#3,163,308
of 7,584,550 outputs
Outputs from Journal of Translational Medicine
#530
of 1,727 outputs
Outputs of similar age
#106,864
of 267,865 outputs
Outputs of similar age from Journal of Translational Medicine
#32
of 89 outputs
Altmetric has tracked 7,584,550 research outputs across all sources so far. This one has received more attention than most of these and is in the 56th percentile.
So far Altmetric has tracked 1,727 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.3. This one has gotten more attention than average, scoring higher than 63% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 267,865 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 58% of its contemporaries.
We're also able to compare this research output to 89 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 57% of its contemporaries.