Prenatal screening service for fetal RHD genotyping to guide prophylaxis: the two-year experience of the Friuli Venezia Giulia region in Italy.

Background: Fetal RHD genotyping of cell-free fetal DNA (cff-DNA) from RhD-negative pregnant women can be used to guide anti-D prophylaxis: the knowledge of fetal RhD type can direct and restrict the use of prenatal anti-D immunoglobulin exclusively to RhD-negative women carrying a RhD-positive fetus. Since November 2019 in the region of Friuli Venezia Giulia (Italy) a prenatal screening service has been offered to RhD-negative women at 22-24 weeks of gestation.

Materials And Methods: The cff-DNA is extracted from a simple peripheral maternal blood sample to analyze the fetal RHD gene: the results are interpreted as RHD-positive fetus, RHD-negative fetus, or Inconclusive.

Innovations in the field of fungal biofilms: looking for new targets and new chemical compounds.

Biofilms pose a serious problem for public health. Penetration of pharmacological agents within a biofilm is hampered by the morphological structure of such microbial communities. A biofilm infection therefore entails adverse outcomes both in the field of cost management and patient prognosis.

Bloodstream infection with Oligella ureolytica: a case report and review of the literature.

Oligella ureolytica is an emerging bacteria rarely implicated as a human pathogen. It is mostly recovered from urinary and respiratory tract specimens as a commensal organism, but very seldom from bloodstream infections. It is rarely reported in the literature, probably due to misidentification of the organism or uncertainty of its pathogenicity.

Mast cells, basophils and B cell connection network.

It has been proven that both resting and activated mast cells (MCs) and basophils are able to induce a significant increase in proliferation and survival of naïve and activated B cells, and their differentiation into antibody-producing cells. The immunological context in which this regulation occurs is of particular interest and the idea that these innate cells induce antibody class switching and production is increasingly gaining ground. This direct role of MCs and basophils in acquired immunity requires cell to cell contact as well as soluble factors and exosomes.

Mast cells enhance proliferation of B lymphocytes and drive their differentiation toward IgA-secreting plasma cells.

The evidence of a tight spatial interaction between mast cells (MCs) and B lymphocytes in secondary lymphoid organs, along with the data regarding the abundance of MCs in several B-cell lymphoproliferative disorders prompted us to investigate whether MCs could affect the proliferation and differentiation of B cells. To this aim, we performed coculture assays using mouse splenic B cells and bone marrow-derived MCs. Both nonsensitized and activated MCs proved able to induce a significant inhibition of cell death and an increase in proliferation of naive B cells.

CD4+CD25+ regulatory T cells suppress mast cell degranulation and allergic responses through OX40-OX40L interaction.

T regulatory (Treg) cells play a role in the suppression of immune responses, thus serving to induce tolerance and control autoimmunity. Here, we explored whether Treg cells influence the immediate hypersensitivity response of mast cells (MCs). Treg cells directly inhibited the FcvarepsilonRI-dependent MC degranulation through cell-cell contact involving OX40-OX40L interactions between Treg cells and MCs, respectively.

APE/Ref-1 makes fine-tuning of CD40-induced B cell proliferation.

Apurinic/apyrimidinic endonuclease-1/Redox factor-1, a multifunctional DNA base excision repair and redox regulation enzyme, plays an important role in oxidative signalling, transcription factor regulation, and cell cycle control. Recently, we have demonstrated that following the triggering of CD40 on B cells, APE/Ref-1 translocates from the cytoplasm to the nucleus and regulates the activity of B cell-specific transcription factors. In the present paper we investigate whether APE/Ref-1 plays a role in controlling CD40-mediated B cell proliferation too.

TRAF2 and p38 are involved in B cells CD40-mediated APE/Ref-1 nuclear translocation: a novel pathway in B cell activation.

The interaction between CD40 and its ligand CD40L plays a key role in the regulation of B cell proliferation, activation, isotype switching and the humoral memory response. APE/Ref-1 plays a key role in transcriptional responses during CD40-mediated B cell activation. It is demonstrated that CD40 signaling is mediated principally through TRAF adapter proteins.

Cooperative activity of Ref-1/APE and ERp57 in reductive activation of transcription factors.

ERp57, a protein disulfide isomerase localized mainly in the endoplasmic reticulum, has also been found in lesser amounts in the cytosol and nucleus, where its function is still not characterized. We report here that ERp57 displays affinity for Ref-1, a protein involved in DNA repair as well as in the reduction and activation of transcription factors. Immunoprecipitation experiments showed that Ref-1 and ERp57 also interact in vivo in at least three types of cultured human cells, namely HepG2, M14, and Raji.

CD40 stimulation induces Pax5/BSAP and EBF activation through a APE/Ref-1-dependent redox mechanism.

CD40 is a member of the growing tumor necrosis factor receptor family that has been shown to play important roles in T cell-mediated B lymphocyte activation. Ligation of B cell CD40 by CD154, mainly expressed on activated T cells, stimulates B cell proliferation, differentiation, isotype switching, up-regulation of surface molecules contributing to antigen presentation, development of the germinal center, and the humoral memory response. In this study we demonstrate that the redox factor APE/Ref-1 acts as a key signaling intermediate in response to CD40-mediated B cell activation.