Toll-Like Receptor and Inflammasome Signals Converge to Amplify the Innate Bactericidal Capacity of T Helper 1 Cells Investigators showed that CD4+ T helper 1 (Th1) cells could be rapidly stimulated by microbe-associated molecular patterns during active infection with Salmonella or Chlamydia. Further, maximal stimulation of Th1 cells by lipopolysaccharide did not require T-cell-intrinsic expression of toll-like receptor 4, interleukin-1 receptor (IL-1R), or interferon-γ receptor but instead required IL-18R, IL-33R, and adaptor protein MyD88. [Immunity] Abstract | Press Release | Graphical Abstract The Cytokine IL-22 Promotes Pathogen Colonization by Suppressing Related Commensal Bacteria Scientists showed that IL-22 has a unique role during infection in that its expression suppressed the intestinal microbiota and enhanced the colonization of a pathogen. IL-22 induced the expression of antimicrobial proteins, including lipocalin-2 and calprotectin, which sequester essential metal ions from microbes. [Immunity] Abstract | Press Release | Graphical Abstract Humanized-BLT Mouse Model of Kaposi’s Sarcoma-Associated Herpesvirus Infection The authors aimed to determine whether the humanized BLT (bone marrow, liver, and thymus) mouse model generated from NOD/SCID/IL2rγ mice can be a useful model for studying Kaposi’s sarcoma-associated herpesvirus infection. [Proc Natl Acad Sci USA] Abstract Rheumatoid Arthritis Patients Exhibit Impaired Candida albicans-Specific Th17 Responses Scientists aimed to examine the relationship between rheumatoid arthritis and susceptibility to C. albicans because of the increasing interest in CD4+ T cell subset (Th17) cells and IL-17 in driving autoimmunity, and the advent of new biologics that target this pathway. [Arthritis Res Ther] Abstract | Full Article HIV Interleukin-7 Signaling Defects in Naive CD4+ T Cells of HIV Patients with CD4+ T Cell Deficiency on Antiretroviral Therapy Associated with T Cell Activation and Senescence Researchers examined the relationship of defects in interleukin (IL)-7 induced naive CD4+ T-cell homeostasis with residual immune activation and CD4+ T-cell senescence in HIV patients receiving antiretroviral therapy who exhibit persistent CD4+ T cell deficiency. [AIDS] Abstract Direct Non-Productive HIV-1 Infection in a T-Cell Line Is Driven by Cellular Activation State and NFkappaB Investigators used a recently described, doubly fluorescent HIV-1 latency model to dissect the role of proviral integration sites and cellular activation state on direct non-productive infections at the single cell level. Proviral integration site mapping of infected Jurkat T-cells revealed that productively and non-productively infected cells are indistinguishable in terms of genomic landmarks, surrounding epigenetic landscapes, and proviral orientation relative to host genes. [Retrovirology] Abstract | Full Article Slow Turnover of HIV-1 Receptors on Quiescent CD4+ T Cells Causes Prolonged Surface Retention of gp120 Immune Complexes In Vivo The authors investigated the turnover of viral receptors (VRs) on peripheral quiescent CD4+ T cells (qCD4s), which are the most abundant peripheral blood CD4+ T cells. Utilizing pharmacological and immunological approaches, they found that the turnover of VRs on qCD4s is extremely slow. [PLoS One] Full Article Fusion of Ubiquitin to HIV Gag Impairs Human Monocyte-Derived Dendritic Cell Maturation and Reduces Ability to Induce Gag T Cell Responses To develop an improved T cell vaccine for HIV scientists investigated whether fusing the ubiquitin gene to the N terminus of the HIV gag gene enhanced targeting to the proteasome resulting in better CD8 T cell responses. [PLoS One] Full Article Win a $25 Amazon Gift Card! Connexon Creative is evaluating reader interest in a new social media platform. Fill out this quick survey for your chance to win 1 of 4 $25 gift cards! Take survey here |