Early Secreted Antigen ESAT-6 of Mycobacterium tuberculosis Promotes Protective T Helper 17 Cell Responses in a Toll-Like Receptor-2-dependent Manner
Published 2011 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Early Secreted Antigen ESAT-6 of Mycobacterium tuberculosis Promotes Protective T Helper 17 Cell Responses in a Toll-Like Receptor-2-dependent Manner
Authors
Keywords
Tuberculosis, Mycobacterium tuberculosis, Immune response, Cell differentiation, Cytokines, Vaccines, T cells, T helper cells
Journal
PLoS Pathogens
Volume 7, Issue 11, Pages e1002378
Publisher
Public Library of Science (PLoS)
Online
2011-11-11
DOI
10.1371/journal.ppat.1002378
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Mycobacterium bovis Bacille Calmette-Guerin Infection in the CNS Suppresses Experimental Autoimmune Encephalomyelitis and Th17 Responses in an IFN- -Independent Manner
- (2014) J. Lee et al. JOURNAL OF IMMUNOLOGY
- Membrane-Bound IL-22 after De Novo Production in Tuberculosis and Anti-Mycobacterium tuberculosis Effector Function of IL-22+ CD4+ T Cells
- (2011) G. Zeng et al. JOURNAL OF IMMUNOLOGY
- T Cells from Programmed Death-1 Deficient Mice Respond Poorly to Mycobacterium tuberculosis Infection
- (2011) Sultan Tousif et al. PLoS One
- TLR2 deficiency by compromising p19 (IL-23) expression limits Th 17 cell responses to Mycobacterium tuberculosis
- (2010) Maria Teixeira-Coelho et al. INTERNATIONAL IMMUNOLOGY
- Pathological role of interleukin 17 in mice subjected to repeated BCG vaccination after infection withMycobacterium tuberculosis
- (2010) Andrea Cruz et al. JOURNAL OF EXPERIMENTAL MEDICINE
- Up-regulated microRNA-146a negatively modulate Helicobacter pylori-induced inflammatory response in human gastric epithelial cells
- (2010) Zhen Liu et al. MICROBES AND INFECTION
- Mycobacterium tuberculosis evades host immunity by recruiting mesenchymal stem cells
- (2010) S. Raghuvanshi et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- ESX/type VII secretion systems and their role in host–pathogen interaction
- (2009) Roxane Simeone et al. CURRENT OPINION IN MICROBIOLOGY
- The role of cytokines in the initiation, expansion, and control of cellular immunity to tuberculosis
- (2009) Andrea M. Cooper et al. IMMUNOLOGICAL REVIEWS
- MicroRNA in the immune system, microRNA as an immune system
- (2009) Li-Fan Lu et al. IMMUNOLOGY
- TB vaccines: current status and future perspectives
- (2009) Claus Aagaard et al. IMMUNOLOGY AND CELL BIOLOGY
- Toll-like Receptor 2 and DC-SIGNR1 Differentially Regulate Suppressors of Cytokine Signaling 1 in Dendritic Cells duringMycobacterium tuberculosisInfection
- (2009) Varsha Srivastava et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- miR-146a Is Critical for Endotoxin-induced Tolerance
- (2009) Md A. Nahid et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Mycobacterium bovis Bacillus Calmette-Guerin Killed by Extended Freeze-Drying Targets Plasmacytoid Dendritic Cells To Regulate Lung Inflammation
- (2009) M. Lagranderie et al. JOURNAL OF IMMUNOLOGY
- Identification of miR-145 and miR-146a as mediators of the 5q– syndrome phenotype
- (2009) Daniel T Starczynowski et al. NATURE MEDICINE
- A multi-valent vaccinia virus-based tuberculosis vaccine molecularly adjuvanted with interleukin-15 induces robust immune responses in mice
- (2009) Pin-Yu Perera et al. VACCINE
- IL-23 and IL-17 in tuberculosis
- (2008) Shabaana A. Khader et al. CYTOKINE
- Delayed protection by ESAT-6–specific effector CD4+T cells after airborneM. tuberculosisinfection
- (2008) Alena M. Gallegos et al. JOURNAL OF EXPERIMENTAL MEDICINE
- Role of M. tuberculosis RD-1 region encoded secretory proteins in protective response and virulence
- (2008) Niladri Ganguly et al. TUBERCULOSIS
Find Funding. Review Successful Grants.
Explore over 25,000 new funding opportunities and over 6,000,000 successful grants.
ExplorePublish scientific posters with Peeref
Peeref publishes scientific posters from all research disciplines. Our Diamond Open Access policy means free access to content and no publication fees for authors.
Learn More