Document Detail


Inefficient lymph node sensitization during respiratory viral infection promotes IL-17-mediated lung pathology.
MedLine Citation:
PMID:  20805422     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Development of bronchus-associated lymphoid tissue has been suggested to enhance local antiviral immune responses; however, ectopic lymph node formation often corresponds to chronic inflammatory diseases. These studies investigated the role of ectopic pulmonary lymph nodes upon respiratory syncytial virus (RSV) infection using CCR7-deficient mice, which develop bronchus-associated lymphoid tissue early in life. CCR7(-/-) mice exhibited impaired secondary lymph node formation, enhanced effector T cell responses and pathogenic mucus production in the lung after RSV infection. IL-17 production from CD4 T cells in CCR7(-/-) mice was most remarkably enhanced. Wild-type animals reconstituted with CCR7(-/-) bone marrow recapitulated the pathogenic lung phenotype in CCR7(-/-) mice, whereas CCR7(-/-) animals reconstituted with wild-type bone marrow had normal lymph node development, diminished IL-17 production and reduced lung pathology. Mixed bone marrow chimeras revealed an alteration of immune responses only in CCR7(-/-) T cells, suggesting that impaired trafficking promotes local effector cell generation. Lymphotoxin-α-deficient mice infected with RSV were used to further examine locally induced immune responses and demonstrated increased mucus production and amplified cytokine responses in the lung, especially IL-17. Neutralization of IL-17 in CCR7(-/-) or in lymphotoxin-α-deficient animals specifically inhibited mucus hypersecretion and reduced IL-13. Thus, immune cell trafficking to secondary lymph nodes is necessary for appropriate cytokine responses to RSV as well as modulation of the local environment.
Authors:
Lara E Kallal; Adam J Hartigan; Cory M Hogaboam; Matthew A Schaller; Nicholas W Lukacs
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-08-30
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-22     Completed Date:  2010-10-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4137-47     Citation Subset:  AIM; IM    
Affiliation:
Department of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Separation
Chemotaxis, Leukocyte / immunology*
Choristoma / immunology,  metabolism
Flow Cytometry
Interleukin-17 / biosynthesis,  immunology*
Lung Diseases / immunology,  virology
Lymph Nodes*
Mice
Mice, Inbred C57BL
Mice, Knockout
Mucus / metabolism
Receptors, CCR7 / deficiency,  genetics,  immunology
Respiratory Syncytial Virus Infections / immunology*,  pathology*
Respiratory Syncytial Viruses
Reverse Transcriptase Polymerase Chain Reaction
T-Lymphocytes / immunology,  metabolism
Grant Support
ID/Acronym/Agency:
AI036302/AI/NIAID NIH HHS; AI073876/AI/NIAID NIH HHS; R01 AI036302-14/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Ccr7 protein, mouse; 0/Interleukin-17; 0/Receptors, CCR7

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


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