STAT1 Controls the Functionality of Influenza-Primed CD4 T Cells but Therapeutic STAT4 Engagement Maximizes Their Antiviral Impact.

It is generally accepted that influenza A virus (IAV) infection promotes a Th1-like CD4 T cell response and that this effector program underlies its protective impact. Canonical Th1 polarization requires cytokine-mediated activation of the transcription factors STAT1 and STAT4 that synergize to maximize the induction of the "master regulator" Th1 transcription factor, T-bet. Here, we determine the individual requirements for these transcription factors in directing the Th1 imprint primed by influenza infection in mice by tracking virus-specific wild-type or T-bet-deficient CD4 T cells in which STAT1 or STAT4 is knocked out.

Intermediate Levels of Pre-Existing Protective Antibody Allow Priming of Protective T Cell Immunity against Influenza.

Overcoming interfering impacts of pre-existing immunity to generate universally protective influenza A virus (IAV)-specific T cell immunity through vaccination is a high priority. In this study, we passively transfer varied amounts of H1N1-IAV-specific immune serum before H1N1-IAV infection to determine how different levels of pre-existing Ab influence the generation and protective potential of heterosubtypic T cell responses in a murine model. Surprisingly, IAV nucleoprotein-specific CD4 and CD8 T cell responses are readily detected in infected recipients of IAV-specific immune serum regardless of the amount transferred.

Bona Fide Th17 Cells without Th1 Functional Plasticity Protect against Influenza.

Optimal transcriptional programming needed for CD4 T cells to protect against influenza A virus (IAV) is unclear. Most IAV-primed CD4 T cells fit Th1 criteria. However, cells deficient for the Th1 "master regulator," T-bet, although marked by reduced Th1 identity, retain robust protective capacity.

Toll-like Receptor 4 Single-Nucleotide Polymorphisms and Heart Transplant Rejection.

Background: Transplant rejection is one of the major problems after heart transplantation (HTx). The aim of the study was to find possible links between chosen single-nucleotide polymorphisms (SNPs) of Toll-like receptor 4 (TLR4) and heart transplant rejection.

Material And Methods: Blood samples were taken from 24 patients subjected to HTx between 2010 and 2016 at the Clinic of Cardiac Surgery and Transplantation and under the control of I Clinic of Cardiology.

Patients' knowledge of heart failure and their perception of the disease.

Purpose: The aim of this study was to gain a deeper insight into patients' perception of chronic heart failure (CHF) symptoms by analyzing their compliance with nonpharmacological recommendations.

Patients And Methods: This was a prospective, single-center survey-based registry. Patients included in this study were hospitalized between December 2014 and January 2016 at the 1 Department of Cardiology, University Hospital of Lord's Transfiguration, Poznań University of Medical Sciences, and had been diagnosed with CHF at least 3 months prior to inclusion.