Role of the cellular transcription factor YY1 in the latent-lytic switch of Kaposi's sarcoma-associated herpesvirus.

Lytic cycle reactivation of Kaposi's sarcoma-associated herpesvirus (KSHV) is initiated by expression of the ORF50 gene. Here we show that YY1 protein specifically binds to the ORF50 promoter (ORF50p) region in vitro and in vivo. After treatment with chemical inducers, including sodium butyrate (SB) and TPA, the levels of YY1 protein are inversely correlated with the lytic induction of KSHV in cells.

Transcriptional regulation of the ORF61 and ORF60 genes of Kaposi's sarcoma-associated herpesvirus.

The ORF61 and ORF60 genes of Kaposi's sarcoma-associated herpesvirus (KSHV) encode the ribonucleotide reductase large and small subunits, respectively. Here we show that ORF50 protein, a latent-lytic switch transactivator, activates the transcription of these two early-lytic genes through different mechanisms. Activation of the ORF61 promoter by ORF50 protein is dependent on an intact RBP-Jkappa-binding site within the identified responsive element and the expression of RBP-Jkappa protein in cells.

Construction and characterization of a novel fusion protein consisting of anti-CD3 antibody fused to recombinant interleukin-2.

T cells can be activated in vitro by monoclonal antibodies to CD3 (anti-CD3) to become non-MHC restricted killer cells (CD3-AK). Anti-CD3 activation upregulates the expression of the interleukin (IL)-2 receptors on T cells whose expansion is facilitated by IL-2. The therapeutic effect of in vivo administration of anti-CD3 and IL-2 has been investigated in many types of human cancers.

Clonal restriction of the expansion of antigen-specific CD8+ memory T cells by transforming growth factor-{beta}.

Recent evidence showed that transforming growth factor-beta (TGF-beta) regulates the global expansion of CD8+ T cells, which are CD44hi, a marker for memory cells. However, it is not clear whether this regulatory mechanism also applies to the antigen-specific CD8+ memory cells. By using a murine mixed lymphocyte culture (MLC) model, we examined the effect of TGF-beta on antigen-specific CD8+ memory cells [cytotoxic T lymphocyte (CTL)].

Inducing long-term survival with lasting anti-tumor immunity in treating B cell lymphoma by a combined dendritic cell-based and hydrodynamic plasmid-encoding IL-12 gene therapy.

In a previous study we showed that immunization with dendritic cells (DC) pulsed with idiotype (Id) fused with CD40 ligand (CD40L) could break the tolerance to Id which is expressed on B lymphoma cells and restored the responsiveness of T(h) cells, and, subsequently, induced IgG antibody response. However, this treatment had no therapeutic effect. In the present study, we found that using a hydrodynamic transfection-based technique, a high level of IL-12 production was noticed as early as 7 h after administering plasmid encoding IL-12 (pIL-12) and persisted at a detectable level for at least 9 days.