Elimination of Mother-to-Infant Transmission of Hepatitis B Virus: 35 Years of Experience.

Chronic hepatitis B viral (HBV) infection remains a major health threat, especially in high-prevalence areas. Most infants infected by mother-to-infant HBV transmission become chronic carriers. In Taiwan, many important preventive interventions have been implemented to block the perinatal transmission of HBV in the past 35 years.

Identification of microRNAs that Regulate the MAPK Pathway in Human Cumulus Cells from PCOS Women with Insulin Resistance.

Polycystic ovary syndrome (PCOS) is one of the most common gynaecological endocrine disorders, and more than 60% of PCOS patients have varying degrees of insulin resistance (IR). The regulatory role of microRNAs (miRNAs) at post-transcriptional levels in human cumulus cells relating to IR in PCOS remains unclear. In this case-control study, 26 PCOS patients with IR (PCOS-IR) and 24 patients without IR (PCOS-control) were enrolled.

Liver-resident NK cells suppress autoimmune cholangitis and limit the proliferation of CD4 T cells.

Liver-resident NK cells are distinct from conventional NK cells and play an important role in the maintenance of liver homeostasis. How liver-resident NK cells participate in autoimmune cholangitis remains unclear. Here, we extensively investigated the impact of NK cells in the pathogenesis of autoimmune cholangitis utilizing the well-established dnTGFβRII cholangitis model, NK cell-deficient (Nfil3) mice, adoptive transfer and in vivo antibody-mediated NK cell depletion.

Prognostic parameters of pediatric acute liver failure and the role of plasma exchange.

Background: This study investigated the prognostic parameters and beneficial effects of repeat plasma exchange in children with acute liver failure (ALF).

Methods: Twenty-three patients under 18 years of age admitted to National Taiwan University Hospital due to ALF from 2003 to 2016 were included in this retrospective analysis.

Results: Among the patients, 11 (48%) had native liver recovery (NLR), 9 (39.

Vitamin D level affects IVF outcome partially mediated via Th/Tc cell ratio.

Problem: The role of vitamin D (VD) in IVF outcome and immune parameters has not been elucidated well.

Method Of Study: Women undergoing IVF treatment with GnRH agonist (Agonist) and progestin-primed ovarian stimulation (PPOS) protocols were divided into VD lower (VDL, 25(OH)VD ≤20 ng/mL) and VD higher (VDH, 25(OH)VD >20 ng/mL) groups. Follicular fluid (FF) VD level, IVF outcomes, and peripheral blood immunophenotypes by flow cytometry were analyzed.

Successful treatment of murine autoimmune cholangitis by parabiosis: Implications for hematopoietic therapy.

There is a significant unmet need in the treatment of primary biliary cirrhosis (PBC) despite significant data on the effector pathways that lead to biliary duct damage. We focused attention on a murine model of PBC, the dominant negative transforming growth factor β receptor II (Tg) mice. To further define the pathways that lead to biliary pathology in these mice, we developed Tg mice deleted of CD4 cells (CD4(-/-)Tg).

Thymic B cells promote thymus-derived regulatory T cell development and proliferation.

Thymic CD4(+) FoxP3(+) regulatory T (Treg) cells are critical for the development of immunological tolerance and immune homeostasis and requires contributions of both thymic dendritic and epithelial cells. Although B cells have been reported to be present within the thymus, there has not hitherto been a definition of their role in immune cell development and, in particular, whether or how they contribute to the Treg cellular thymic compartment. Herein, using both phenotypic and functional approaches, we demonstrate that thymic B cells contribute to the maintenance of thymic Treg cells and, using an in vitro culture system, demonstrate that thymic B cells contribute to the size of the thymic Treg compartment via cell-cell MHC II contact and the involvement of two independent co-stimulatory pathways that include interactions between the CD40/CD80/CD86 co-stimulatory molecules.

γ-Glutamyl transpeptidase level as a screening marker among diverse etiologies of infantile intrahepatic cholestasis.

Objectives: Low γ-glutamyl transpeptidase (GGT) level is an important marker for progressive familial intrahepatic cholestasis, yet the cutoff level and clinical application is not well defined. This study aimed to evaluate the role of GGT as a screening marker among diverse etiologies of infantile cholestasis.

Methods: This retrospective study analyzed 256 cholestatic infants admitted to a tertiary referral center between 2000 and 2012.

Differential modulation by IL-17A of Cholangitis versus Colitis in IL-2Rα deleted mice.

IFN-γ is a signature Th1 cell associated cytokine critical for the inflammatory response in autoimmunity with both pro-inflammatory and potentially protective functions. IL-17A is the hallmark of T helper 17 (Th17) cell subsets, produced by γδT, CD8+ T, NK and NKT cells. We have taken advantage of our colony of IL-2Rα-/- mice that spontaneously develop both autoimmune cholangitis and inflammatory bowel disease.

Distinct from its canonical effects, deletion of IL-12p40 induces cholangitis and fibrosis in interleukin-2Rα(-/-) mice.

The IL-12 family modulates T cell mediated autoimmune diseases and GWAS in PBC have suggested a critical role of IL-12 and its subunits in modulating portal inflammation. We have taken advantage of an aggressive model of portal inflammation and colitis in IL-2Rα(-/-) mice to study the specific role of IL-12 and, in particular, the immunobiology of p40(-/-)IL-2Rα(-/-) mice. Colonies of IL-2Rα(+/-), IL-2Rα(-/-) and p40(-/-)IL-2Rα(-/-) mice were studied for the natural history of immunopathology in liver and colon using histology and immunohistochemistry.

STAT3-mediated attenuation of CCl4-induced mouse liver fibrosis by the protein kinase inhibitor sorafenib.

There have been major advances in defining the immunological events associated with fibrosis in various chronic liver diseases. We have taken advantage of this data to focus on the mechanisms of action of a unique multi-kinase inhibitor, coined sorafenib, on CCl4-induced murine liver fibrosis, including the effects of this agent in models of both acute and chronic CCl4-mediated pathology. Importantly, sorafenib significantly attenuated chronic liver injury and fibrosis, including reduction in liver inflammation and histopathology as well as decreased expression of liver fibrosis-related genes, including α-smooth muscle actin, collagen, matrix metalloproteinases and the tissue inhibitor of metalloproteinase-1.