Frida Arrey

ORCID: 0000-0003-4543-4219
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • Viral-associated cancers and disorders
  • T-cell and B-cell Immunology
  • Immunotherapy and Immune Responses
  • Tuberculosis Research and Epidemiology
  • Lymphoma Diagnosis and Treatment
  • Endoplasmic Reticulum Stress and Disease
  • Mosquito-borne diseases and control
  • Hematopoietic Stem Cell Transplantation
  • Polyomavirus and related diseases
  • Diagnosis and treatment of tuberculosis
  • Immune Response and Inflammation
  • Chemokine receptors and signaling
  • Cytomegalovirus and herpesvirus research
  • Mycobacterium research and diagnosis
  • Autophagy in Disease and Therapy

Max Planck Institute for Infection Biology
2014-2019

Max Planck Society
2014

Rockefeller University
2007-2010

CEA Paris-Saclay - Etablissement de Fontenay-aux-roses
2009

Commissariat à l'Énergie Atomique et aux Énergies Alternatives
2009

Infectious Disease Models and Innovative Therapies
2009

University of Birmingham
2009

University of Bern
2009

Global Viral
2008

Many pathogens that cause human disease infect only humans. To identify the mechanisms of immune protection against these and also to evaluate promising vaccine candidates, a small animal model would be desirable. We demonstrate primary T cell responses in mice with reconstituted system components control infection oncogenic persistent Epstein-Barr virus (EBV). These cytotoxic interferon-γ–producing were leukocyte antigen (HLA) restricted specific for EBV-derived peptides. In HLA-A2...

10.1084/jem.20081720 article EN The Journal of Experimental Medicine 2009-06-01

Successful host defense against numerous pulmonary infections depends on bacterial clearance by polymorphonuclear leukocytes (PMNs); however, excessive PMN accumulation can result in life-threatening lung injury. Local expression of CXC chemokines is critical for recruitment. The impact chemokine-dependent recruitment during Mycobacterium tuberculosis infection not fully understood. Here, we analyzed genes encoding M. tuberculosis–infected murine tissue and found that promotes upregulation...

10.1172/jci72030 article EN Journal of Clinical Investigation 2014-02-09

Cells of the innate immune system act in synergy to provide a first line defense against pathogens. Here we describe that dendritic cells (DCs), matured with viral products or mimics thereof, including Epstein-Barr virus (EBV), activated natural killer (NK) more efficiently than other mature DC preparations. CD56(bright)CD16(-) NK cells, which are enriched human secondary lymphoid tissues, responded primarily this activation. DCs elicited 50-fold stronger interferon-gamma (IFN-gamma)...

10.1371/journal.ppat.0040027 article EN cc-by PLoS Pathogens 2008-02-05

DCs activate NK cells during innate immune responses to viral infections. However, the composition and kinetics of immunological synapse mediating this interaction are largely unknown. Here, we report rapid formation an between human resting mature DCs. Although inhibitory cell receptors were polarized synapse, where they known protect from lysis, also received activation signals that induced mobilization intracellular calcium CD69 upregulation. The high-affinity component receptor for...

10.1172/jci31751 article EN Journal of Clinical Investigation 2007-10-19

Epstein Barr virus (EBV) causes lymphomas in immune competent and, at increased frequencies, compromised patients. In the presence of an intact system, EBV-associated express most cases only 3 or fewer EBV antigens protein level, always including nuclear antigen 1 (EBNA1). EBNA1 is a prominent target for EBV-specific CD4(+) T cell and humoral responses healthy carriers. Here we demonstrate that patients with lymphomas, primarily Hodgkin's lymphoma, lack detectable EBNA1-specific T-cell have...

10.1002/ijc.23845 article EN International Journal of Cancer 2008-09-09
Coming Soon ...