RGD Reference Report - Toll-like receptor 6 drives interleukin-17A expression during experimental hypersensitivity pneumonitis. - Rat Genome Database

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Toll-like receptor 6 drives interleukin-17A expression during experimental hypersensitivity pneumonitis.

Authors: Fong, DJ  Hogaboam, CM  Matsuno, Y  Akira, S  Uematsu, S  Joshi, AD 
Citation: Fong DJ, etal., Immunology. 2010 May;130(1):125-36. Epub 2010 Jan 11.
RGD ID: 4889532
Pubmed: PMID:20070409   (View Abstract at PubMed)
PMCID: PMC2855800   (View Article at PubMed Central)
DOI: DOI:10.1111/j.1365-2567.2009.03219.x   (Journal Full-text)

Hypersensitivity pneumonitis (HP) is a T-cell-driven disease that is histologically characterized by diffuse mononuclear cell infiltrates and loosely formed granulomas in the lungs. We have previously reported that interleukin-17A (IL-17A) contributes to the development of experimental HP, and that the pattern recognition receptor Toll-like receptor 6 (TLR6) might be a factor in the initiation of this response. Using a well-established murine model of Saccharopolyspora rectivirgula-induced HP, we investigated the role of TLR6 in the immunopathogenesis of this disease. In the absence of TLR6 signalling, mice that received multiple challenges with S. rectivirgula-antigen (SR-Ag) had significantly less lung inflammation compared with C57BL/6 mice (wild-type; WT) similarly challenged with SR-Ag. Flow cytometric analysis of whole lung samples from SR-Ag-challenged mice showed that TLR6(-/-) mice had a decreased CD4(+) : CD8(+) T-cell ratio compared with WT mice. Cytokine analysis at various days after the final SR-Ag challenge revealed that whole lungs from TLR6(-/-) mice contained significantly less IL-17A than lungs from WT mice with HP. The IL-17A-driving cytokines IL-21 and IL-23 were also expressed at lower levels in SR-Ag-challenged TLR6(-/-) mice, when compared with SR-Ag-challenged WT mice. Other pro-inflammatory cytokines, namely interferon-gamma and RANTES, were also found to be regulated by TLR6 signalling. Anti-TLR6 neutralizing antibody treatment of dispersed lung cells significantly impaired SR-Ag-induced IL-17A and IL-6 generation. Together, these results indicate that TLR6 plays a pivotal role in the development and severity of HP via its role in IL-17A production.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
extrinsic allergic alveolitis  ISOTlr6 (Mus musculus)4889532; 4889532 RGD 
extrinsic allergic alveolitis  IMP 4889532 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Tlr6  (toll-like receptor 6)

Genes (Mus musculus)
Tlr6  (toll-like receptor 6)

Genes (Homo sapiens)
TLR6  (toll like receptor 6)


Additional Information