CURRENT PUBLICATIONS (Ranked by Impact Factor of the Journal)
Reduction of Disulphide Bonds Unmasks Potent Antimicrobial Activity of Human Beta-Defensin 1 Defensins, characterized by three intramolecular disulphide-bridges, are key effector molecules of innate immunity that protect the host from infectious microbes and shape the composition of microbiota at mucosal surfaces. Herein researchers show that after reduction of disulphide-bridges human beta-defensin 1 becomes a potent antimicrobial peptide against the opportunistic pathogenic fungus Candida albicans and against anaerobic, Gram-positive commensals of Bifidobacterium and Lactobacillus species. [Nature] Discovery of a Viral NLR Homolog that Inhibits the Inflammasome The viral homolog subverts the function of cellular NLRs (nucleotide binding and oligomerization, leucine-rich repeat), which suggests that modulation of NLR-mediated innate immunity is important for the lifelong persistence of herpes viruses. [Science] IRF5 Promotes Inflammatory Macrophage Polarization and TH1-TH17 Responses Here researchers show that IRF5 expression in macrophages was reversibly induced by inflammatory stimuli and contributed to the plasticity of macrophage polarization. [Nat Immunol] Erythropoietin Contrastingly Affects Bacterial Infection and Experimental Colitis by Inhibiting Nuclear Factor-B-Inducible Immune Pathways Here, researchers show that erythropoietin (EPO) inhibits the induction of proinflammatory genes including tumor necrosis factor (TNF)-alpha and inducible nitric oxide synthase in activated macrophages, which is mechanistically attributable to blockage of nuclear factor (NF)-kappaB p65 activation by EPO. [Immunity] Two-Stage Cooperative T Cell Receptor-Peptide Major Histocompatibility Complex-CD8 Trimolecular Interactions Amplify Antigen Discrimination The T cell receptor and CD8 bind peptide-major histocompatibility complex glycoproteins to initiate adaptive immune responses, yet the trimolecular binding kinetics at the T cell membrane is unknown. By using a micropipette adhesion frequency assay, researchers show that this kinetics has two stages. [Immunity] T Lymphocytes Negatively Regulate Lymph Node Lymphatic Vessel Formation Lymph node lymphatic vessels (LNLVs) serve as a conduit to drain antigens from peripheral tissues to within the lymph nodes. LNLV density is known to be positively regulated by vascular endothelial growth factors secreted by B cells, macrophages, and dendritic cells (DCs). Here, researchers show that LNLV formation was negatively regulated by T cells. [Immunity] Posttranscriptional Silencing of Effector Cytokine mRNA Underlies the Anergic Phenotype of Self-Reactive T Cells Self-reactive T cell clones that escape negative selection are either deleted or rendered functionally unresponsive (anergic), thus preventing them from propagating host tissue damage. By using an in vivo model, researchers investigated molecular mechanisms for T cell tolerance, finding that despite a characteristic inability to generate effector cytokine proteins, self-reactive T cells express large amounts of cytokine mRNAs. [Immunity] Maternal T cells Limit Engraftment After In Utero Hematopoietic Cell Transplantation in Mice Here, researchers have demonstrated that there is macrochimerism of maternal leukocytes in the blood of unmanipulated mouse fetuses, with substantial increases in T cell trafficking after in utero hematopoietic cell transplantation. [J Clin Invest] Expression of p16INK4a Prevents Cancer and Promotes Aging in Lymphocytes Here, using somatic, tissue-specific inactivation of the p16INK4a tumor suppressor in murine T- or B-lymphoid progenitors, researchers report that ablation of p16INK4a can either rescue aging or promote cancer in a lineage-specific manner. [Blood] Two Distinct Auto-Regulatory Loops Operate at the PU.1 Locus in B cells and Myeloid Cells Researchers previously identified an upstream regulatory cis-element (URE) whose targeted deletion in mice decreases PU.1 expression and causes leukemia. Researchers show here that the URE alone is insufficient to confer physiological PU.1 expression, but requires the cooperation with other, previously unidentified elements. [Blood]
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