Ji‐Hun Mo

3-Hydroxyanthranilic acid (HAA), a compound generated during tryptophan metabolism initiated by indoleamine 2,3-dioxygenase, is known to induce T cell death, but its molecular target is not known. Here we report that HAA inhibits NF-kappaB activation upon T cell antigen receptor engagement by specifically targeting PDK1. Inhibition of NF-kappaB by HAA leads to dysfunction and cell death of activated Th2 cells, which in turn suppresses experimental asthma. Inhibition of NF-kappaB and induction of apoptosis is specific to CD4 T cells because HAA does not inhibit NF-kappaB activation or induce cell death upon Toll-like receptor 4 stimulation in dendritic cells. Thus, HAA is a natural inhibitor that restrains T cell expansion and activation.

BACKGROUND: Thyroid fine-needle aspiration (FNA) is used as a screening test of choice for evaluation of thyroid nodules. However, approximately 15% to 25% of the cases are classified as indeterminate, posing dilemmas in decision-making. This study was designed to compare the diagnostic performances of second FNA and core needle biopsy of indeterminate nodules by initial FNA. METHODS: From February 2005 through June 2009, 258 patients who completed scheduled follow-ups were enrolled and the follow-up results were analyzed. RESULTS: Nondiagnostic results were obtained in 41.8% of the second FNA group and in 1.7% of the core needle biopsy group (p < .001; chi-square). The nodules that show borderline features in preoperative ultrasonography had a malignancy rate of 18.3% and could be identified successfully with core needle biopsy. CONCLUSION: Core needle biopsy is a better method for evaluating indeterminate nodules by initial FNA than second FNA, especially in patients with ultrasonographic findings of a borderline nodule.

We explored the physiological role of conventional dendritic cells (cDCs) in acute colitis induced by a single cycle of dextran sodium sulfate administration. Depending on their mode of activation and independently of T cells, cDCs can enhance or attenuate the severity of dextran sodium sulfate-induced colitis. The latter beneficial effect was achieved, in part, by IFN-1 induced by Toll-like receptor 9-activated cDCs. IFN-1 inhibits colonic inflammation by regulating neutrophil and monocyte trafficking to the inflamed colon and restraining the inflammatory products of tissue macrophages. These data highlight a novel role of cDCs in the regulation of other innate immune cells and position them as major players in acute colonic inflammation.