Elena Priceputu

ORCID: 0000-0002-7362-0804
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Research Areas
  • HIV Research and Treatment
  • Immune Cell Function and Interaction
  • Immune cells in cancer
  • T-cell and B-cell Immunology
  • HIV/AIDS drug development and treatment
  • Immune Response and Inflammation
  • Mast cells and histamine
  • Immunotherapy and Immune Responses
  • Cytokine Signaling Pathways and Interactions
  • Nuclear Receptors and Signaling
  • interferon and immune responses
  • Renal Diseases and Glomerulopathies
  • Amyloidosis: Diagnosis, Treatment, Outcomes
  • Reproductive System and Pregnancy
  • Virus-based gene therapy research
  • Herpesvirus Infections and Treatments
  • Hepatitis B Virus Studies
  • Developmental Biology and Gene Regulation
  • Infectious Diseases and Mycology
  • vaccines and immunoinformatics approaches
  • Macrophage Migration Inhibitory Factor
  • TGF-β signaling in diseases

Montreal Clinical Research Institute
2000-2023

MRC Laboratory of Molecular Biology
2005-2013

Universität Hamburg
2001

CD4(+)- and CD8(+)-T-cell death is a frequent immunological dysfunction associated with the development of human AIDS. We studied murine model AIDS, CD4C/HIV transgenic (Tg) mouse model, to assess importance apoptotic pathway in immunodeficiency virus type 1 (HIV-1) pathogenesis. In these Tg mice, Nef major determinant disease expressed immature mature CD4(+) T cells macrophage/myeloid lineage. report here novel AIDS-like phenotype: enhanced death, most likely by apoptosis (as assessed...

10.1128/jvi.79.10.6377-6391.2005 article EN Journal of Virology 2005-04-27

ABSTRACT We previously reported that CD4C/human immunodeficiency virus (HIV) Nef transgenic (Tg) mice, expressing in CD4 + T cells and of the macrophage/dendritic cell (DC) lineage, develop a severe AIDS-like disease, characterized by depletion cells, as well lung, heart, kidney diseases. In order to determine contribution distinct populations hematopoietic development this five additional Tg strains through restricted cell-specific regulatory elements were generated. These express DCs,...

10.1128/jvi.00125-09 article EN Journal of Virology 2009-07-16

Abstract —In the present study, we demonstrate γ-interferon (γ-IFN)–inducible scavenger receptor A (SR-A) mRNA expression during early stages of THP-1 and blood monocyte differentiation. Predominant induction SR-A type II parallels increased accumulation cholesteryl esters under these conditions. potential signal transducer activator transcription (STAT1) binding site (γ-interferon activation site) in promoter demonstrates γ-IFN–inducible DNA activity is most likely responsible for...

10.1161/01.atv.21.5.825 article EN Arteriosclerosis Thrombosis and Vascular Biology 2001-05-01

The cellular and molecular mechanisms of dysfunction depletion CD4+ T lymphocytes over the course human immunodeficiency virus type 1 (HIV-1) infection are still incompletely understood, but chronic immune activation is thought to play an important role in disease progression. We studied T-cell biology CD4C/HIV transgenic (Tg) mice, which Nef expression sufficient induce a severe AIDS-like including preferential decrease cells. show here that Nef-expressing Tg cells exhibit...

10.1128/jvi.78.10.5244-5257.2004 article EN Journal of Virology 2004-04-28

ABSTRACT We previously reported that the human immunodeficiency virus type 1 NL4-3 Nef is necessary and sufficient to induce a severe AIDS-like disease in transgenic (Tg) mice when protein expressed under regulatory sequences of CD4 gene. have now assayed additional alleles (SF2, JR-CSF, YU10x, [T71R] alleles), including some from long-term nonprogressors (AD-93, 032an, 039nm alleles) same Tg system compared their pathogenicities. All these downregulated cell surface cells vitro also, with...

10.1128/jvi.02691-06 article EN Journal of Virology 2007-02-22

Human immunodeficiency virus (HIV) or simian (SIV) infection causes myelodysplasia, anemia, and accumulation of inflammatory monocytes (CD14+ CD16+) through largely unknown cellular molecular pathways. The mouse cells thought to be equivalent human CD14+ CD16+ are CD11b+ Gr1+ myeloid-derived suppressor (MDSC). We used HIV transgenic (Tg) models study MDSC, namely, CD4C/Nef Tg mice expressing nef in dendritic (DC), pDC, CD4+ T, other mature immature myeloid CD11c/Nef with a more restricted...

10.1128/jvi.00471-21 article EN cc-by Journal of Virology 2021-06-13

HIV-1 infection causes depletion and/or dysfunction of distinct CD4(+) T cell subsets and may affect these differently. Using the CD4C/HIV-1(Nef) transgenic (Tg) mice as a model, we report that Nef total cells, but preserves relatively enriches regulatory cells (Treg). We found Nef-mediated Treg enrichment is direct result expression in occurs independently Nef-induced lymphopenia, most likely results from multiple mechanisms: lower apoptosis, enhanced division, increased generation...

10.4049/jimmunol.1203272 article EN The Journal of Immunology 2014-01-25

Abstract We previously found that provirus insertion in T cell tumors of mouse mammary tumor virus/c-myc transgenic (Tg) mice induced two forms Notch1 mutations. Type I mutations generated truncated molecules, one intracellular (IC) (Notch1IC) and extracellular (Notch1EC), while type II was deleted its C terminus (Notch1ΔCT). expressed these mutants Tg using the CD4 promoter. Both Notch1IC Notch1ΔCT, but not Notch1EC, developed double-positive (DP) thymomas. These disseminated more...

10.4049/jimmunol.177.4.2153 article EN The Journal of Immunology 2006-08-15
Ιωάννα Αγγελετοπούλου Markos Marangos Stelios F. Assimakopoulos Αthanasia Mouzaki Konstantinos Thomopoulos and 95 more Christos Triantos Masafumi Miyai Toru Iwama Akira Hara Hiroyuki Tomita Kangyun Wu Yong Zhang Stephen Austin Huiqing Yin‐Declue Derek E. Byers Erika C. Crouch Michael J. Holtzman Erin E. Ball Christopher C. Weiss Hongwei Liu Kenneth A. Jackson M. Kevin Keel Christopher A. Miller Koen K. A. Van Rompay Lark L. Coffey Patricia A. Pesavento Chunyan Hu Elena Priceputu Marc Cool Pavel Chrobák Nathalie Bouchard Clara Forestier Clifford A. Lowell Serge Bénichou Zaher Hanna Virginie Royal Paul Jolicoeur Ying Li Jian Dai Fuyuki Kametani Masahide Yazaki Akihito Ishigami Masayuki Mori Hiroki Miyahara Keiichi Higuchi Valeria Fridman D’Alessandro Corina N. D’Alessandro‐Gabazza Taro Yasuma Masaaki Toda Atsuro Takeshita Atsushi Tomaru Suphachai Tharavecharak Isaiah O. Lasisi Rebecca Hess Kota Nishihama Hajime Fujimoto Tetsu Kobayashi Isaac Cann Esteban C. Gabazza Po-Chun Chen Chien-Peng Hsu Sheng-Ya Wang Tsai-Yen Wu Yu-Jyun Lin You-Tzung Chen Shu‐Hao Hsu Zhijie Shi Jingyi Zhu Liheng Yu Xiaopeng Li Jiaxin Li Huyan Chen Lianjun Chen Joshua Levy John P. Zavras Eren M. Veziroglu Mustafa Nasir-Moin Fred Kolling Brock C. Christensen Lucas A. Salas Rachael E. Barney Scott Palisoul Bing Ren Xiaoying Liu Darcy A. Kerr Kelli B. Pointer Gregory Tsongalis Louis Vaickus Matthew B. Carson Amy J. Warner Vincenza L. Geiser Jessica D. Hathaway‐Schrader Alexander V. Alekseyenko Julie Marshall Caroline Westwater Chad M. Novince Natalia A. Vilchinskaya Wooi K. Lim С. П. Белова Thomas C. Roberts

10.1016/s0002-9440(23)00138-4 article EN publisher-specific-oa American Journal Of Pathology 2023-06-01
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