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Background  Pulmonary dendritic cells drive lung responses to foreign antigens, including  Saccharopolyspora rectivirgula , a causative agent of hypersensitivity pneumonitis. While the airway inflammatory mechanisms involved in hypersensitivity pneumonitis are well described, the mechanisms leading to the break in homeostasis and hypersensitivity pneumonitis onset are not well-described, and could involve CD103 +  dendritic cells, which are found at baseline and during inflammatory responses in the lung. However, recent demonstration of the ability of CD103 +  dendritic cells to induce inflammatory responses starkly contrasts with their classically described role as regulatory cells. These discrepancies may be attributable to the lack of current information on the importance of CD103 expression and modulation on these cells during inflammatory episodes.    Methods  To verify the importance of CD103 expression in the regulation of hypersensitivity pneumonitis, wild-type and  Cd103   -/-   mice were exposed intranasally to  S .  rectivirgula  and airway inflammation was quantified. Surface expression of CD103 in response to  S .  rectivirgula  exposure was studied and cell transfers were used to determine the relative importance of CD103 expression on dendritic cells and T cells in regulating the inflammation in hypersensitivity pneumonitis.    Results   Cd103   -/-   mice developed an exacerbated inflammatory response as early as 18h following  S .  rectivirgula  exposure. CD103 expression on dendritic cells was downregulated quickly following  S .  rectivirgula  exposure, and cell transfers demonstrated that CD103 expression on dendritic cells specifically (and not T cells) regulates the onset and severity of this response.    Conclusion  All in all, we demonstrate that CD103 expression by dendritic cells, but not T cells, is crucial for homeostasis maintenance and the regulation of the T H 17 airway inflammatory response in hypersensitivity pneumonitis.

Hypersensitivity pneumonitis onset and severity is regulated by CD103 dendritic cell expression