Spontaneous rupturing of splenic artery aneurysm: Another reason for fatal syncope and shock (Case report and literature review).

Splenic artery aneurysm (SAA) is a rare condition; however, it is one of the most common intra-abdominal aneurysm. In the emergency department (ED), due to an uncommon cause of shock and syncope in SAA, it poses great diagnostic challenge for emergency physicians. Here we reported a case of spontaneous rupturing of SAA.

FDG-PET/CT Assessment of the Cerebral Protective Effects of Hydrogen in Rabbits with Cardiac Arrest.

Background: Anatomical imaging methods and histological examinations have limited clinical value for early monitoring of brain function damage after cardiac arrest (CA) in vivo.

Objective: We aimed to assess the cerebral protective effects of hydrogen in rabbits with CA by using fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT).

Methods: Male rabbits were divided into the hydrogen-treated (n=6), control (n=6), and sham (n=3) groups.

[Application of positron emission tomography in detection of myocardial glucose metabolism in rabbit cardiac arrest models].

To investigate the changes of myocardial glucose metabolism in rabbit cardiac arrest models and the effect of hydrogen intervention by 18F-fluroro-2-deoxyglucose (18F-FDG) positron emission tomography (PET) imaging.
 Methods: Fifteen male New Zealand white rabbits were randomly divided into a hydrogen group (n=6), a control group (n=6) and a sham group (n=3). Cardiac arrest (CA) was induced by intravenous injection of potassium chloride.

Herpesvirus saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor.

Herpesvirus Saimiri gene 13 (HVS13) exhibits 57% identity with the predicted sequence of a T cell-derived molecule termed CTLA8. Recombinant HVS13 and CTLA8 stimulate transcriptional factor NF-kappaB activity and Interleukin-6 (IL-6) secretion in fibroblasts, and costimulate T cell proliferation. An HVS13.

Expression of IFNalpha-inducible genes and modulation of HLA-DR and thyroid stimulating hormone receptors in Graves' disease.

Interferon alpha (IFNalpha) plays an important role in the pathogenesis of different autoimmune diseases. IFNalpha is widely used for the treatment of chronic viral infections, particularly chronic hepatitis C virus infection; however, several case reports have emerged describing autoimmune conditions, such as Graves' disease (GD), that have developed in the patients receiving IFNalpha. The mechanism by which IFNalpha is involved in GD remains poorly understood.

Regulation of TLR7/9 responses in plasmacytoid dendritic cells by BST2 and ILT7 receptor interaction.

Plasmacytoid dendritic cells (pDCs) produce copious type I interferon (IFN) upon sensing nucleic acids through Toll-like receptor (TLR) 7 and TLR9. Uncontrolled pDC activation and IFN production are implicated in lymphopenia and autoimmune diseases; therefore, a mechanism controlling pDC IFN production is essential. Human pDCs specifically express an orphan receptor, immunoglobulin-like transcript 7 (ILT7).

Modulation of Notch signaling by antibodies specific for the extracellular negative regulatory region of NOTCH3.

The Notch pathway regulates the development of many tissues and cell types and is involved in a variety of human diseases, making it an attractive potential therapeutic target. This promise has been limited by the absence of potent inhibitors or agonists that are specific for individual human Notch receptors (NOTCH1-4). Using an unbiased functional screening, we identified monoclonal antibodies that specifically inhibit or induce activating proteolytic cleavages in NOTCH3.

IL-25 augments type 2 immune responses by enhancing the expansion and functions of TSLP-DC-activated Th2 memory cells.

Interleukin (IL) 25 (IL-17E), a distinct member of the IL-17 cytokine family, plays important roles in evoking T helper type 2 (Th2) cell-mediated inflammation that features the infiltrations of eosinophils and Th2 memory cells. However, the cellular sources, target cells, and underlying mechanisms remain elusive in humans. We demonstrate that human Th2 memory cells expressing distinctive levels of IL-25 receptor (R) are one of the responding cell types.

A new mechanism regulating the initiation of allergic airway inflammation.

Background: The earliest immune events induced by allergens are poorly understood, yet are likely essential to understanding how allergic inflammation is established.

Objective: We sought to describe the earliest signaling events activated by allergen and determine their significance to allergic inflammation.

Methods: A fungal-associated allergenic proteinase (FAP) or ovalbumin was administered once intranasally to wild-type mice to determine their ability to induce allergy-associated genes and initiate allergic lung inflammation.

Maintenance and polarization of human TH2 central memory T cells by thymic stromal lymphopoietin-activated dendritic cells.

The identity of TH2 memory cells and the mechanism regulating their maintenance during allergic inflammation remain elusive. We report that circulated human CD4+ T cells expressing the prostaglandin D2 receptor (CRTH2) are TH2 central memory T cells, characterized by their phenotype, TH2 cytokine production, gene-expression profile, and the ability to respond to allergens. Only dendritic cells (DCs) activated by thymic stromal lymphopoietin (TSLP) can induce a robust expansion of CRTH2+CD4+ TH2 memory cells, while maintaining their central memory phenotype and TH2 commitments.

Plasmacytoid dendritic cell-specific receptor ILT7-Fc epsilonRI gamma inhibits Toll-like receptor-induced interferon production.

Immunoglobulin-like transcripts are a family of inhibitory and stimulatory cell surface immune receptors. Transcripts for one member of this family, ILT7, are selectively expressed in human plasmacytoid dendritic cells (pDCs). We demonstrate here that ILT7 protein associates with the signal adapter protein Fc epsilonRI gamma to form a receptor complex.

Mast cell and immune inhibitory receptors.

Modulation by balancing activating and inhibitory receptors constitutes an important mechanism for regulating immune responses. Cells that are activated following ligation of receptors bearing immunoreceptor tyrosine-based activation motifs (ITAMs) can be negatively regulated by other receptors bearing immuno-receptor tyrosine-based inhibition motifs (ITIMs). Human mast cells (MCs) are the major effector cells of type I hypersensitivity and important participants in a number of disease processes.

TSLP-activated dendritic cells induce an inflammatory T helper type 2 cell response through OX40 ligand.

We recently showed that dendritic cells (DCs) activated by thymic stromal lymphopoietin (TSLP) prime naive CD4(+) T cells to differentiate into T helper type 2 (Th2) cells that produced high amounts of tumor necrosis factor-alpha (TNF-alpha), but no interleukin (IL)-10. Here we report that TSLP induced human DCs to express OX40 ligand (OX40L) but not IL-12. TSLP-induced OX40L on DCs was required for triggering naive CD4(+) T cells to produce IL-4, -5, and -13.

Identification and expression of a new type II transmembrane protein in human mast cells.

A cDNA encoding a new type II transmembrane protein has been isolated from human mast cells by subtraction cloning. This cDNA contains an open reading frame of 186 amino acids. RT-PCR analysis showed that this gene is differentially expressed in mast cells.

Amphiregulin expression in human mast cells and its effect on the primary human lung fibroblasts.

Background: Amphiregulin is a member of the epidermal growth factor family and has been shown to stimulate the proliferation of human keratinocytes in an autocrine manner.

Objective: The aim of the present study was to examine the expression change of growth factors, especially amphiregulin, in human mast cells induced by IgE cross-linking.

Methods: Microarray analysis and RT-PCR were used to analyze the gene expression profile of human cord blood-derived mast cells (CBMCs) stimulated with IgE cross-linking.

The SH3 domain-containing adaptor HIP-55 mediates c-Jun N-terminal kinase activation in T cell receptor signaling.

HIP-55 (hematopoietic progenitor kinase 1 (HPK1)-interacting protein of 55 kDa, also called SH3P7 and mAbp1) is a novel SH3 domain-containing protein. HIP-55 binds to actin filaments both in vitro and in vivo. HIP-55 activates HPK1 and c-Jun N-terminal kinase (JNK), which are two important lymphocyte signaling molecules.

Regulation of activin A expression in mast cells and asthma: its effect on the proliferation of human airway smooth muscle cells.

Activin A, a homodimeric protein (betaAbetaA) and a member of the TGF-beta superfamily, is involved in the inflammatory repair process. Using cDNA microarray analysis, we discovered strong induction of the activin betaA gene in human mast cells (MC) on stimulation with PMA and calcium ionophore (A23187). Activin betaA mRNA was also highly induced in primary cultured murine bone marrow MC (BMMC) after stimulation by IgE receptor cross-linking.

Calcineurin/nuclear factors of activated T cells (NFAT)-activating and immunoreceptor tyrosine-based activation motif (ITAM)-containing protein (CNAIP), a novel ITAM-containing protein that activates the calcineurin/NFAT-signaling pathway.

We report in this study the identification and characterization of a novel protein that we designated as calcineurin/NFAT-activating and immunoreceptor tyrosine-based activation motif (ITAM)-containing protein (CNAIP). The predicted 270-amino acid sequence contains an N-terminal signal peptide, an immunoglobin domain in the extracellular region, a transmembrane domain and an ITAM in the cytoplasmic tail. Quantitative reverse transcription-PCR showed that CNAIP was preferentially expressed in neutrophils, monocytes, mast cells, and other immune-related cells.