The transcription factor T-bet regulates the differentiation of CD4(+) T-helper type 1 (Th1) cells and represses Th2 lineage commitment. Since Th1 cells are crucial in the defense against pathogens, several studies addressed the role of T-bet in immunity to infection using T-bet knockout (T-bet(-/-)) mice. Nevertheless, it is still unclear whether T-bet is required for defense. Although vaccini...

all-trans retinoic acid (atra), as an active metabolite of vitamin a, has been shown to affect immune cells. this study was performed to evaluate the effect of atra on viability, proliferation, activation and lineage-specific transcription factors of cd4+ t cells. cd4+ t cells were  separated  from  heparinized  blood  of  healthy  donors  and  were  cultured  in conditions, some with, some wit...

Upregulation of genes for interferon (IFN)-γ and CXC chemokine receptor (CXCR)3 expression, two crucial molecules in sarcoid inflammation and granuloma formation, is directly controlled by the T-helper (Th)1 transcription factor T-bet (T-box, expressed in T-cells). However, there is no information on T-bet expression in sarcoidosis or its relationship with "sarcoidosis-associated" genes. Theref...

An inappropriate balance between T-helper (Th)1 and Th2 cytokine production underlies inflammatory changes that result in airway disease. Expression of the T-box transcription factor T-bet regulates differentiation of Th cells and production of Th1 cytokines, particularly IFNγ. T-bet-deficient mice develop airway hyperreactivity, undergo airway remodeling, and exhibit defects in IFNγ production...

The T-box transcription factor T-bet is expressed in a number of hematopoetic cell types and plays an essential role in the lineage determination of Th1 T-helper cells. In the absence of T-bet, CD4(+) T-cells fail to induce IFNgamma, the cytokine whose expression characterizes Th1 cells. Here we show that, surprisingly, T-bet induces the expression of endogenous IFNgamma in non-immune human cel...

As a means of developing therapies that target the pathogenic T cells in multiple sclerosis (MS) without compromising the immune system or eliciting systemic side effects, we investigated the use of T-bet-specific antisense oligonucleotides and small interfering RNAs (siRNA) to silence T-bet expression in autoreactive encephalitogenic T cells and evaluated the biological consequences of this su...

In this issue of the Journal, Dorfman and colleagues1 describe the usefulness of T-bet as a marker for specific subtypes of B-cell lymphoma. T-bet originally was identified as a T-box family transcription factor that dominantly programs CD4 and CD8 T-cell development along Th1 and Tc1 pathways, respectively.2 It accomplished this impressive task in part through the coordinated transcriptional a...

Cell-mediated adaptive immunity is very important in tumor immune surveillance and tumor vaccination. However, the genetic program underlying an effective adaptive antitumor immunity is elusive. T-bet and Eomesodermin (Eomes) have been suggested to be master regulators of Th1 cells and CD8(+) T cells. However, whether they are important for T cell-mediated antitumor immunity is controversial. I...

Given the association with autoimmune disease, there is great interest in defining cellular factors that limit overactive or misdirected Th17-type inflammation. Using in vivo and in vitro models, we investigated the molecular mechanisms for cytokine-mediated inhibition of Th17 responses, focusing on the role of STAT1 and T-bet in this process. These studies demonstrate that, during systemic inf...

T-bet is a transcription factor of the T-box family that regulates the expression of numerous immune system-associated genes. T-bet directs the acquisition of the Th1-associated genetic program in differentiating CD4(+) lymphocytes. It also influences the development of NK and NKT cells through its regulation of the IL-2/IL-15Rbeta-chain (CD122) and the trafficking of these lymphocytes through ...