Skip to content
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
immunology and microbiology
IFNAR1 controls progression to cerebral malaria in children and CD8
+
T cell brain pathology in plasmodium berghei-infected mice
Journal of Immunology, Volume 190, No. 10, Year 2013
Notification
URL copied to clipboard!
Description
Development of cerebral malaria (CM), a severe and fatal form of clinical Plasmodium falciparum infection, results from a damaging cascade of vascular, inflammatory, and immunological host responses that leads to brain injury. Progression to CM can be modified by host genetic factors. Our case-control study in Angolan children aimed at highlighting the role of IFN (a, b) receptor 1 (IFNAR1) in progression to CM. We report a robust association between IFNAR1 and CM protection, as well as detailed studies showing analogous protection from experimental CM in Ifnar1-/- mice infected with P. berghei ANKA. We developed a novel cell-transfer protocol that enables spleen cell priming in the absence of disease. This led to the discovery that IFNAR1 expression in CD8+ T cells is crucial and can abrogate resistance to experimental CM in Ifnar1 -/- mice. Splenic CD8+ T cells from Ifnar1-/- mice are functionally activated upon infection, yet are unable to mediate experimental CM development within the brain tissue. Our findings prove that IFNAR1 signaling unleashes CD8+ T cell effector capacity, which is vital for CM, and raises the hypothesis that the cohesive role of IFNAR1 in both human and mouse CM operates through CD8+ T cell triggering. © 2013 by The American Association of Immunologists, Inc.
Authors & Co-Authors
Ball, Elizabeth Ann
Portugal, Oeiras
Instituto Gulbenkian de Ciência
Sambo, Maria Rosario
Portugal, Oeiras
Instituto Gulbenkian de Ciência
Angola, Luanda
University Agostinho Neto
Angola, Luanda
Hospital Pediátrico David Bernardino
Martins, Madalena
Portugal, Oeiras
Instituto Gulbenkian de Ciência
Portugal, Lisbon
Universidade de Lisboa
Trovoada, Maria Jesus
Portugal, Oeiras
Instituto Gulbenkian de Ciência
Sao Tome and Principe
Centro National de Endemias
Benchimol, Carla
Angola, Luanda
Hospital Pediátrico David Bernardino
Costa, João Pedro
Portugal, Oeiras
Instituto Gulbenkian de Ciência
Goncalves, Ligia Antunes
Portugal, Oeiras
Instituto Gulbenkian de Ciência
Coutinho, António A.
Portugal, Oeiras
Instituto Gulbenkian de Ciência
Penha-Gonçalves, Carlos
Portugal, Oeiras
Instituto Gulbenkian de Ciência
Statistics
Citations: 53
Authors: 9
Affiliations: 5
Identifiers
Doi:
10.4049/jimmunol.1300114
ISSN:
00221767
e-ISSN:
15506606
Research Areas
Genetics And Genomics
Infectious Diseases
Maternal And Child Health
Violence And Injury
Study Design
Case-Control Study