Allergic manifestations in women with silicone breast implants.

Introduction: Silicone breast implants (SBI) result in immune dysregulation and are associated with autoimmune diseases. Recently, we reported dysregulated levels of IgG autoantibodies directed against G protein-coupled receptors (GPCRs) of the autonomic nervous system which were linked to the autoimmune dysautonomia in silicone breast implant illness (SBII).

Aims: We aimed to explore the possible association between allergy with dysregulated IgE autoantibodies directed against GPCRs of the autonomic nervous system in women with SBI.

Tumor-Derived Extracellular Vesicles Induce CCL18 Production by Mast Cells: A Possible Link to Angiogenesis.

Mast cells (MCs) function as a component of the tumor microenvironment (TME) and have both pro- and anti-tumorigenic roles depending on the tumor type and its developmental stage. Several reports indicate the involvement of MCs in angiogenesis in the TME by releasing angiogenic mediators. Tumor cells and other cells in the TME may interact by releasing extracellular vesicles (EVs) that affect the cells in the region.

Extracellular Vesicles as Emerging Players in Intercellular Communication: Relevance in Mast Cell-Mediated Pathophysiology.

Mast cells are major effector cells in eliciting allergic responses. They also play a significant role in establishing innate and adaptive immune responses, as well as in modulating tumor growth. Mast cells can be activated upon engagement of the high-affinity receptor FcεRI with specific IgE to multivalent antigens or in response to several FcεRI-independent mechanisms.

Lung cancer-derived extracellular vesicles: a possible mediator of mast cell activation in the tumor microenvironment.

Activated mast cells are often found in the tumor microenvironment. They have both pro- and anti-tumorigenic roles, depending on the tumor type. Several lines of evidence suggest that the tumor microenvironment contains multiple soluble factors that can drive mast cell recruitment and activation.

MicroRNA Involvement in Allergic and Non-Allergic Mast Cell Activation.

Allergic inflammation is accompanied by the coordinated expression of numerous genes and proteins that initiate, sustain, and propagate immune responses and tissue remodeling. MicroRNAs (miRNAs) are a large class of small regulatory molecules that are able to control the translation of target mRNAs and consequently regulate various biological processes at the posttranscriptional level. MiRNA profiles have been identified in multiple allergic inflammatory diseases and in the tumor microenvironment.

Characterization of chronic urticaria and associated conditions in a large population of adolescents.

Background: Although chronic spontaneous urticaria (CSU) affects all age groups, data regarding CSU in adolescents is scarce.

Objective: To characterize the epidemiology, demographics, and comorbidities associated with CSU in a large, cross-sectional nationwide population of adolescents.

Methods: Medical records of 16-year-old candidate conscripts to the Israeli Defense Forces were reviewed.

MicroRNA-4443 regulates mast cell activation by T cell-derived microvesicles.

Background: The mechanism by which mast cells (MCs) are activated in T cell-mediated inflammatory processes remains elusive. Recently, we have shown that microvesicles derived from activated T cells (mvT*s) can stimulate MCs to degranulate and release several cytokines.

Objective: The aim of this study was to characterize the contribution of microRNAs (miRs) delivered by microvesicles to MC activation.

Pathogenesis and Pathology of Mastocytosis.

Systemic mastocytosis is a clonal disorder of mast cells that may variably present with characteristic skin lesions, episodes of mast cell mediator release, and disturbances of hematopoiesis. No curative therapy presently exists. Conventional management has relied on agents that antagonize mediators released by mast cells, inhibit mediator secretion, or modulate mast cell proliferation.

The Involvement of Protein Kinase D in T Cell-Induced Mast Cell Activation.

Background: It has recently been reported that mast cells (MC) can be activated to degranulate and release certain cytokines in response to direct physical contact with activated but not resting T cells or their membranes. The MAPK family members ERK and p38 were found to participate. In this work, we further characterize the signaling events involved in this novel pathway of activation.

Increased Prevalence of Diabetes Mellitus in a Non-Obese Adult Population: HIV-Infected Ethiopians.

Background: Diabetes mellitus (DM) is a metabolic sequel in people infected with HIV, especially following the advent of HAART. This may be a particular concern in immigrants due to lifestyle changes.

Objectives: To characterize the prevalence of DM in HIV-infected Ethiopians in Israel, and to define the risk factors.

[NON-CLONAL MAST CELL ACTIVATION SYNDROME: DESCRIPTION OF SERIES OF PATIENTS, DIAGNOSTIC CRITERIA AND TREATMENT].

A non-clonal mast cell activation syndrome is a newly emerged diagnosis. It shares the clinical features of anaphylaxis and mastocytosis despite having distinct mast cell biology. In this,paper we describe a series of patients representing the spectrum of non-clonal mast cell activation syndrome (nc-MCAS).

Integrating innate and adaptive immune cells: Mast cells as crossroads between regulatory and effector B and T cells.

A diversity of immune mechanisms have evolved to protect normal tissues from infection, but from immune damage too. Innate cells, as well as adaptive cells, are critical contributors to the correct development of the immune response and of tissue homeostasis. There is a dynamic "cross-talk" between the innate and adaptive immunomodulatory mechanisms for an integrated control of immune damage as well as the development of the immune response.

T cell-derived microvesicles induce mast cell production of IL-24: relevance to inflammatory skin diseases.

Background: It has recently been shown that microvesicles derived from activated T cells can stimulate human mast cells (MCs) to degranulate and release several cytokines.

Objective: The aim of this study was to characterize microvesicle-induced MC expression patterns. Through identification of unique cytokine and chemokine expression, we attempted to reveal pathogenetic roles for this pathway of MC activation.

T cell-mediated modulation of mast cell function: heterotypic adhesion-induced stimulatory or inhibitory effects.

Close physical proximity between mast cells and T cells has been demonstrated in several T cell mediated inflammatory processes such as rheumatoid arthritis and sarcoidosis. However, the way by which mast cells are activated in these T cell-mediated immune responses has not been fully elucidated. We have identified and characterized a novel mast cell activation pathway initiated by physical contact with activated T cells, and showed that this pathway is associated with degranulation and cytokine release.

Increased eosinophilic responses in splenectomized patients.

Background: The spleen is a key organ within the immune system. Its removal is known to bring about adverse effects such as an increased susceptibility to overwhelming infection. Few reports have suggested that the spleen may play a role in controlling eosinophilic responses, mostly based on animal models.

Mast cells as sources and targets of membrane vesicles.

In addition to being major effector cells in the elicitation of allergic responses, mast cells have been found to play a significant role in the establishment of innate and adaptive immune responses. This occurs, in part, by regulating the phenotype and function of immune cells such as T cells, B cells and dendritic cells, and by acting as antigen presenting cells. Indeed, mast cells have been found to be activated in various T cell-mediated inflammatory processes and to reside in close physical proximity to T cells.

Blood pressure modulation following activation of mast cells by cationic cell penetrating peptides.

Short cell penetrating peptides (CPP) are widely used in vitro to transduce agents into cells. But their systemic effect has not been yet studied in detail. We studied the systemic effect of the cell penetrating peptides, penetratin, transportan and pro-rich, on rat hemodynamic functions.

Inhibition of contact sensitivity by farnesylthiosalicylic acid-amide, a potential Rap1 inhibitor.

We hypothesized that Ras proximate 1 (Rap1) functions as an additional target for farnesylthiosalicylic acid (FTS) or its derivatives, and that the inhibition of Rap1 in lymphocytes by these agents may represent a method for treating inflammatory disorders. Indeed, we found that FTS-amide (FTS-A) was able to inhibit the elicitation phase of delayed cutaneous hypersensitivity in vivo. This effect was associated with the inhibition of Rap1 more than with the inhibition of Harvey rat sarcoma viral oncogene (Ras).

Neurologic manifestations as presenting symptoms of endocarditis.

The features of infective endocarditis include both cardiac and non-cardiac manifestations. Neurologic complications are seen in up to 40% of patients with infective endocarditis and are the presenting symptom in a substantial percentage. We describe in detail the clinical scenarios of three patients admitted to our hospital, compare their characteristics and review the recent literature describing neurologic manifestations of infective endocarditis.

Mast cell activation by fibrinogen-related homologous c-terminal peptides (haptides) modulates systemic blood pressure.

Background: Haptides are a family of short peptides homologous to C-termini sequences of fibrinogen chains β and γ (haptides Cβ and preCγ, respectively) which were previously shown to penetrate and bind cells.

Objectives: This work investigates the systemic effect of the haptides with possible clinical implications.

Methods: Intra-arterial monitoring in rats recorded the haptides' effects on systemic blood pressure.

T cell-induced mast cell activation: a role for microparticles released from activated T cells.

Close physical proximity between mast cells and T cells has been demonstrated in several T cell-mediated inflammatory processes. However, the way by which mast cells are activated in these T cell-mediated immune responses has not been fully elucidated. We previously identified and characterized a novel mast cell activation pathway initiated by physical contact with activated T cells and showed that this pathway is associated with degranulation and cytokine release.