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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
Interleukin-17-mediated immunopathogenesis in experimental hypersensitivity pneumonitis
Amrita D Joshi1, Daniel J Fong, Sameer R Oak
1Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-0602, USA.
American Journal of Respiratory and Critical Care Medicine
|January 20, 2009
Summary
Interleukin-17A (IL-17A) drives Saccharopolyspora rectivirgula (SR-Ag)-induced hypersensitivity pneumonitis (HP) by increasing inflammation and CD11c(+) cells. Targeting IL-17A offers a promising therapeutic strategy for HP.
Area of Science:
- Immunology
- Pulmonology
- Microbiology
Background:
- T cells are crucial in Saccharopolyspora rectivirgula-induced hypersensitivity pneumonitis (HP).
- The specific role of Interleukin-17A (IL-17A) in HP pathogenesis remains largely unknown.
- Investigating IL-17A's contribution is vital for understanding HP.
Purpose of the Study:
- To investigate the role of IL-17A in a murine model of SR-Ag-induced HP.
- To determine if IL-17A influences inflammatory responses and cell populations in HP.
Main Methods:
- Experimental HP was induced in wild-type and IL-17 gene-deficient mice via oropharyngeal instillation of SR-Ag.
- Lung homogenates, bronchoalveolar lavage fluid, and ex-vivo lung cultures were analyzed for IL-17 levels.
- Flow cytometry and histological examination were used to assess inflammatory cells and mediators in IL-17-deficient and wild-type mice.
Main Results:
- SR-Ag-induced HP showed increased levels of IFN-gamma, IL-12p35, and IL-17 in lung tissues.
- IL-17-deficient mice exhibited reduced inflammatory cell infiltration, fewer CD11c(+) cells, and lower levels of inflammatory mediators compared to wild-type mice.
- Anti-IL-17 antibody treatment decreased inflammation and CD11c(+) cell populations in HP mice.
Conclusions:
- IL-17A plays a critical role in the immunopathology of SR-Ag-induced HP.
- IL-17A contributes to inflammation and the accumulation of specific immune cells in the lungs.
- Targeting IL-17A presents a potential therapeutic avenue for managing hypersensitivity pneumonitis.
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