Document Detail


IL-17 and Th17 cells in tuberculosis.
MedLine Citation:
PMID:  21075039     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Tuberculosis is primarily a disease of the lung. Constant expression of cellular immunity in this organ is required to control Mycobacterium tuberculosis growth, but this can also result in chronic inflammation and pathologic consequences. During primary tuberculosis both IFN-γ and IL-17 are induced: both are potent inflammatory cytokines capable of inducing expression of chemokines that promote cell recruitment and granuloma organization throughout infection. During the chronic phase, a balance between Th1 and Th17 responses needs to be achieved to control bacterial growth and limit immunopathology, as a shift of the response towards excessive IL-17 production may sustain extensive neutrophil recruitment and tissue damage. Thus, regulation of Th1 and Th17 responses during tuberculosis is essential to promote anti-mycobacterial immunity and prevent extensive immunopathological consequences.
Authors:
Egídio Torrado; Andrea M Cooper
Related Documents :
19237529 - Contribution of flagellin pattern recognition to intestinal inflammation during salmone...
21440589 - Intrinsic apoptotic pathway is subverted in mouse macrophages persistently infected by ...
17568179 - Listeria monocytogenes evades killing by autophagy during colonization of host cells.
19683679 - The s. typhimurium effector sope induces caspase-1 activation in stromal cells to initi...
12975369 - Maturation of lipoproteins by type ii signal peptidase is required for phagosomal escap...
12427099 - Genes in the salmonella pathogenicity island 2 and the salmonella virulence plasmid are...
12606089 - The ambiguous role of immunity in echinococcosis: protection of the host or of the para...
16001169 - Bcl-2-mediated potentiation of neocarzinostatin-induced apoptosis: requirement for casp...
16365459 - Innate stimuli accentuate end-organ damage by nephrotoxic antibodies via fc receptor an...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2010-11-12
Journal Detail:
Title:  Cytokine & growth factor reviews     Volume:  21     ISSN:  1879-0305     ISO Abbreviation:  Cytokine Growth Factor Rev.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-06     Completed Date:  2011-03-11     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  9612306     Medline TA:  Cytokine Growth Factor Rev     Country:  England    
Other Details:
Languages:  eng     Pagination:  455-62     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ltd. All rights reserved.
Affiliation:
Trudeau Institute, Inc., 154 Algonquin Ave., Saranac Lake, NY 12983, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
BCG Vaccine / immunology
Cell Differentiation
Humans
Interferon-gamma / immunology
Interleukin-17 / immunology*
Interleukins / immunology
Lung / immunology
Mice
Th17 Cells / immunology*
Tuberculosis / immunology*,  physiopathology
Grant Support
ID/Acronym/Agency:
AI46530/AI/NIAID NIH HHS; AI67723/AI/NIAID NIH HHS; AI69121/AI/NIAID NIH HHS; P01 AI046530-04/AI/NIAID NIH HHS; R01 AI067723-05/AI/NIAID NIH HHS; R01 AI069121-04/AI/NIAID NIH HHS; R37 AG025805-08/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/BCG Vaccine; 0/Interleukin-17; 0/Interleukins; 0/interleukin-22; 82115-62-6/Interferon-gamma

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Effect of pilates mat exercises and conventional exercise programmes on transversus abdominis and ob...
Next Document:  C-type lectins, fungi and Th17 responses.