LEF-1 negatively controls interleukin-4 expression through a proximal promoter regulatory element.

Lymphoid enhancer-binding factor 1 (LEF-1) and T cell factor (TCF-1) are downstream effectors of the Wnt signaling pathway and are involved in the regulation of T cell development in the thymus. LEF-1 and TCF-1 are also expressed in mature peripheral primary T cells, but their expression is down-regulated following T cell activation. Although the decisive roles of LEF-1 and TCF-1 in the early stages of T cell development are well documented, the functions of these factors in mature peripheral T cells are largely unknown.

Rifampicin induces MDR1 expression in Candida albicans.

Objectives: Overexpression of efflux pumps such as MDR1 has been identified as an important mechanism contributing to fluconazole resistance in Candida albicans. This phenomenon is frequently observed in fluconazole-resistant strains isolated from AIDS patients treated with various pharmaceuticals. Therefore, we hypothesized that some of these compounds might influence the expression of genes responsible for fluconazole resistance.

Wogonin sensitizes resistant malignant cells to TNFalpha- and TRAIL-induced apoptosis.

TNFalpha has previously been used in anticancer therapy. However, the therapeutic application of TNFalpha was largely limited due to its general toxicity and the fact that it activates the NF-kappaB-family transcription factors, which are proinflammatory and antiapoptotic. To overcome this problem in vitro, specific NF-kappaB inhibitors or transcription or protein synthesis inhibitors such as actinomycin D and cycloheximide are usually used in combination to increase TNFalpha killing of tumor cells.

Ultraviolet irradiation suppresses T cell activation via blocking TCR-mediated ERK and NF-kappa B signaling pathways.

UV irradiation is carcinogenic and immunosuppressive. Previous studies indicate that UV-mediated alteration of APCs and induction of suppressor T cells play a critical role in UV-induced immune suppression. In this study, we show that UV irradiation can directly (independently of APCs and suppressor T cells) inhibit T cell activation by blocking TCR-mediated phosphorylation of ERK and IkappaB via overactivation of the p38 and JNK pathways.

Rocaglamide derivatives are immunosuppressive phytochemicals that target NF-AT activity in T cells.

Aglaia (family Meliaceae) plants are used in traditional medicine (e.g., in Vietnam) for the treatment of inflammatory skin diseases and allergic inflammatory disorders such as asthma.

The anti-inflammatory sesquiterpene lactone parthenolide suppresses IL-4 gene expression in peripheral blood T.

Sesquiterpene lactones (SL) derived from Mexican India medicinal plants and parthenolide, the major SL from European feverfew, have raised considerable interest because of their anti-inflammatory and complex pharmacological action. Interleukin-4 (IL-4) is a key cytokine that influences the development of T helper 2 cells and plays an important role in the pathogenesis of allergic diseases. We show here that the anti-inflammatory parthenolide suppresses IL-4 expression at the mRNA and the protein levels in a dose-dependent manner.

Vitamin E inhibits IL-4 gene expression in peripheral blood T cells.

IL-4 plays a pivotal role in the development of allergic inflammation via induction of IgE isotype switching, increase of IgE receptor expression, promoting Th2 cell differentiation, and stimulating several genes involved in atopic disorders. Previous studies in human and mouse models have shown that high vitamin E intake correlates with low IgE concentration and reduced prevalence of allergic reactions. We, therefore, investigated the mechanism of the vitamin E effect on T cells.

Vitamin E inhibits CD95 ligand expression and protects T cells from activation-induced cell death.

Apoptosis is a morphologically distinct form of cell death involved in many physiological and pathological processes. Expression of the CD95 (APO-1/Fas) ligand (CD95L) is critically involved in activation-induced cell death (AICD) of activated T cells. Here we show that the natural free radical scavenger vitamin E suppresses the activity of the transcription factors NF-kappa B and AP-1, thus blocking expression of CD95L and preventing T cell AICD.