Small_CronIn This Issue” highlights articles that are among the top 10% of articles published in the Journal of Immunology.  A corresponding ImmunoCast of “In This Issue” is also produced for each issue and can be found on The Journal of Immunology web site at: http://www.jimmunol.org/rss/jipodcast.xhtml.

Below is the abstract of the paper published from Dr. Cron's laboratory in the September 15 issue of the Journal in Immunology, which was highlighted "In This Issue".

Transcriptional Trouble

HIV-1 preferentially replicates in activated CD4+ T cells that produce Th2 cytokines, but the mechanism driving this preference is not understood. Zhang et al. (p. 2746) hypothesized that Th2-specific transcription factors such as c-maf might drive HIV-1 replication. Single-cell level analysis of human CD4+ T cells in vitro confirmed that IL-4–producing cells preferentially promoted HIV-1 replication and long terminal repeat (LTR)-directed transcription. This preferential replication was not related to chemokine receptor expression, viral tropism, or differences in apoptosis between Th1 and Th2 cells. Instead, the transcription factor c-maf was found to specifically bind to the HIV-1 proximal LTR near the NF-κB and NFAT binding sites. These sites of the HIV-1 LTR were preferentially bound by NFAT2 and NF-κB p65, but not NFAT1 or NF-κB p50. Together with c-maf, NFAT2 and NF-κB p65 cooperatively enhanced transcription at both the IL-4 promoter and the HIV-1 LTR. Small interfering RNA-mediated depletion of c-maf impaired the transcription of both IL-4 and HIV-1 LTR. These results were upheld in primary CD4+ T cells by the observation that the three transcription factors cooperatively augmented HIV-1 expression. These data enhance our understanding of the mechanisms responsible for HIV-1 disease progression and present c-maf as a potential target for therapies aimed at slowing viral replication.

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