Open Access. Powered by Scholars. Published by Universities.®
- Keyword
-
- Department of Microbiology and Immunology (2)
- Thomas Jefferson University (2)
- AKT (1)
- Alpha-fetaprotein (1)
- Animals (1)
-
- Apoptotic (1)
- Bacteria (1)
- Bacterial Proteins (1)
- Biological (1)
- Biological Transport (1)
- CD4+ T lymphocyte; highly active antiretroviral therapy; human; Human immunodeficiency virus; Human immunodeficiency virus infection; immune response; immune restoration; immunomodulation; long terminal repeat; nonhuman; priority journal; review; viremia; virus latency; antivirus agent; virus DNA; virus RNA (1)
- Cell Line (1)
- Chlamydia (1)
- Confocal (1)
- Endocytosis (1)
- Follicular (1)
- Germinal center b cells (1)
- Glycoproteins (1)
- Helper t cells (1)
- Hepatocyte Nuclear Factor 1 (1)
- Immunity (1)
- Immunization (1)
- Kv1.3 (1)
- Legionella (1)
- Liposomes (1)
- Liver (1)
- Mer deficiency (1)
- Microscopy (1)
- Microscopy, Confocal (1)
- Models (1)
- Publication
- Publication Type
- File Type
Articles 1 - 5 of 5
Full-Text Articles in Medical Genetics
Intracellular Bacteria Encode Inhibitory Snare-Like Proteins., Fabienne Paumet, Jordan Wesolowski, Alejandro Garcia-Diaz, Cedric Delevoye, Nathalie Aulner, Howard A Shuman, Agathe Subtil, James E Rothman
Intracellular Bacteria Encode Inhibitory Snare-Like Proteins., Fabienne Paumet, Jordan Wesolowski, Alejandro Garcia-Diaz, Cedric Delevoye, Nathalie Aulner, Howard A Shuman, Agathe Subtil, James E Rothman
Fabienne Paumet
Pathogens use diverse molecular machines to penetrate host cells and manipulate intracellular vesicular trafficking. Viruses employ glycoproteins, functionally and structurally similar to the SNARE proteins, to induce eukaryotic membrane fusion. Intracellular pathogens, on the other hand, need to block fusion of their infectious phagosomes with various endocytic compartments to escape from the degradative pathway. The molecular details concerning the mechanisms underlying this process are lacking. Using both an in vitro liposome fusion assay and a cellular assay, we showed that SNARE-like bacterial proteins block membrane fusion in eukaryotic cells by directly inhibiting SNARE-mediated membrane fusion. More specifically, we showed that …
Signaling Mechanisms Involved In The Generation Of Human Peripheral Itregs, Mary Catherine Reneer
Signaling Mechanisms Involved In The Generation Of Human Peripheral Itregs, Mary Catherine Reneer
Theses and Dissertations--Microbiology, Immunology, and Molecular Genetics
Maintaining balance in the human immune system is critical for the body’s ability to discriminate between foreign and self-antigens. This balance is achieved, in part, by a subpopulation of T cells known as induced regulatory T cells (iTregs). Dysregulation of this population may contribute to the onset and progression of cancer, chronic inflammation and autoimmune diseases. Therefore, manipulation of iTreg development holds promising therapeutic potential; however, studying this vital population has proven difficult due to low numbers, heterogeneous cell populations, substantial phenotypic differences between mouse and human cells, and the high plasticity seen in iTregs. These current limitations have prevented …
Effects Of Apoptotic Cell Accumulation Caused By Mer Deficiency On Germinal Center B Cells And Helper T Cells, Tahsin N. Khan, Eric B. Wong, Ziaur S.M. Rahman
Effects Of Apoptotic Cell Accumulation Caused By Mer Deficiency On Germinal Center B Cells And Helper T Cells, Tahsin N. Khan, Eric B. Wong, Ziaur S.M. Rahman
Department of Microbiology and Immunology Faculty Papers
Mer (MerTK), a member of the Tyro-3/Axl/Mer subfamily receptor tyrosine kinases, expression on phagocytes facilitates their clearance of apoptotic cells (ACs). Mer expression in germinal centers (GCs) occurs predominantly on tingible body macrophages. B and T cells do not express Mer. Mer deficiency (Mer-/-) results in the accumulation of ACs in GCs and augmented antibody-forming cell (AFC), GC and IgG2 Ab responses against T-dependent (TD) Ag. Here, we show that AC accumulation in GCs and elevated AFC, GC and IgG2 Ab responses in Mer-/- mice lasted for at least 80 days after immunization with NP-OVA. Enhanced responses and AC accumulation …
Hiv Rna Suppression And Immune Restoration: Can We Do Better?, Marilia Rita Pinzone, Michelino Di Rosa, Bruno Cacopardo, Giuseppe Nunnari
Hiv Rna Suppression And Immune Restoration: Can We Do Better?, Marilia Rita Pinzone, Michelino Di Rosa, Bruno Cacopardo, Giuseppe Nunnari
Department of Microbiology and Immunology Faculty Papers
HAART has significantly changed the natural history of HIV infection: patients receiving antiretrovirals are usually able to control viremia, even though not all virological responders adequately recover their CD4+ count. The reasons for poor immune restoration are only partially known and they include genetic, demographic and immunologic factors. A crucial element affecting immune recovery is immune activation, related to residual viremia; indeed, a suboptimal virological control (i.e., low levels of plasma HIV RNA) has been related with higher levels of chronic inflammation and all-cause mortality. The sources of residual viremia are not yet completely known, even though the most important …
Regulation Of Hepatic Gene Expression During Liver Development And Disease, Hui Ren
Regulation Of Hepatic Gene Expression During Liver Development And Disease, Hui Ren
Theses and Dissertations--Microbiology, Immunology, and Molecular Genetics
My first project was to investigate the role of Hepatocyte Nuclear Factor 1 (HNF1) and Nuclear Factor I (NFI) on alpha-fetoprotein (AFP) promoter activity during liver development. AFP is highly expressed in the fetal liver, silenced at birth, and remains at very low levels in the adult liver. A GA substitution located at -119 of the human AFP promoter is associated with hereditary persistence of AFP (HPAFP) expression in the adult liver (Hum Molec Genet, 1993, 2:379). The -120 region harbors overlapping binding sites for HNF1 and NFI. While it has been shown that the GA substitution increases HNF1 binding, …