Ibrutinib Is an Irreversible Molecular Inhibitor of ITK Driving a Th1 Selective Pressure in T-Lymphocytes Using ibrutinib clinical trial samples along with well-characterized neoplastic (chronic lymphocytic leukemia), parasitic infection (Leishmania major), and infectious disease (Listeria monocytogenes) models, researchers established ibrutinib as a clinically relevant and physiologically potent interleukin-2 inducible kinase (ITK) inhibitor with broad therapeutic utility. [Blood] Abstract Anticancer Compound ABT-263 Accelerates Apoptosis in Virus-Infected Cells and Imbalances Cytokine Production and Lowers Survival Rates of Infected Mice ABT-263 and its structural analogues ABT-199 and ABT-737 inhibit B-cell lymphoma 2, BCL2L1 long isoform and BCL2L2 proteins and promote cancer cell death. Investigators showed that at non-cytotoxic concentrations, these small molecules accelerate the deaths of non-cancerous cells infected with influenza A virus or other viruses. [Cell Death Dis] Full Article IFN-γ Production by CD27+ NK Cells Exacerbates Listeria monocytogenes Infection in Mice by Inhibiting Granulocyte Mobilization The authors demonstrated that during lethal infection by L. monocytogenes, activation of natural killer (NK) cells via the costimulatory molecule CD27 leads to excessive IFN-γ production. [Eur J Immunol] Abstract | Press Release Neuroimmunomodulation in Human Autoimmune Liver Disease Researchers examined the distribution of intrahepatic NPY, SP immunoreactive nerve fibers and their antomical relationship with immunocells containing tumor necrosis factor-α and nuclear factor κB in patients with autoimmune hepatitis. [Cell Tissue Res] Abstract Self-Adjuvanting Influenza Candidate Vaccine Presenting Epitopes for Cell-Mediated Immunity on a Proteinaceous Multivalent Nanoplatform Scientists exploited the features of a virus-like particle, adenoviral dodecahedron, for engineering a multivalent vaccination platform carrying influenza epitopes for cell-mediated immunity. [Vaccine] Abstract HIV Induction of IL-17 and Nonclassical T-Cell Activation by HIV-Tat Protein The authors found HIV-Tat protein and IL-17-expressing mononuclear cells in the brain of an individual with immune reconstitution inflammatory syndrome. Tat was also present in the CSF of individuals virologically controlled on antiretroviral therapy. Hence, they examined if Tat protein could directly activate T cells. [Proc Natl Acad Sci USA] Abstract Dysregulated Tim-3 Expression on Natural Killer Cells Is Associated with Increased Galectin-9 Levels in HIV-1 Infection Scientists analyzed Tim-3 and Gal-9 expression in a cohort of 85 individuals with early and chronic HIV-1 infection, and in 13 HIV-1 seronegative control subjects. HIV-1 infection was associated with reduced expression of Tim-3 on natural killer cells, which was normalized by HAART. [Retrovirology] Abstract | Press Release Mucosal Th17 Cell Function Is Altered during HIV Infection and Is an Independent Predictor of Systemic Immune Activation HIV infection is characterized by mucosal Th17 depletion, microbial translocation, and immune activation. Therefore, researchers assessed the function of blood and sigmoid Th17 cells during both early and chronic HIV infection, as well as the impact of short- and long-term antiretroviral therapy. [J Immunol] Abstract Emergence of a Distinct HIV-Specific IL-10-Producing CD8+ T-Cell Subset with Immunomodulatory Functions during Chronic HIV-1 Infection Analysis of IL-10 production at the single cell level in 51 chronically infected subjects showed that a subset of CD8+ T cells with a CD25neg FoxP3neg phenotype contributes substantially to IL-10 production in response to HIV-1 gag stimulation. [Eur J Immunol] Abstract Cycloviolacin O2 (CyO2) Suppresses Productive Infection and Augments the Antiviral Efficacy of Nelfinavir in HIV-1 Infected Monocytic Cells Researchers evaluated the potentially therapeutic effects of CyO2 on cell viability, membrane disruption, p24 production, and proviral integration in U1 cells; a monocytic cell model of HIV-1 latency and reactivation. [Biopolymers] Abstract |