Mammary gland (MG) response to bacterial intrusion is driven by the innate immune system, but can be modulated by the adaptive immunity. The model antigen ovalbumin (OVA) has already been shown to induce an antigen-specific inflammatory response when infused into the MG of cows previously sensitized by a systemic immunization but not of control naive cows. The objective of our study was to characterize this immune response. An overexpression of the genes encoding IL-17A, IL-17F, IL-21, IL-22 and INF-γ was found in milk cells and mammary tissue RNA extracts in the early phase of the inflammatory response following intramammary infusion of OVA. At the protein level, IL-17A was detected in milk as soon as 8 h post-challenge, and both IL-17A and IFN-γ concentrations peaked at 12 to 24 h postchallenge. Expression of IL-17A, as revealed by immunohistochemistry, was located in epithelial cells, in leukocytes in the connective tissue and in association with the epithelium, and in migrated alveolar leukocytes of challenged quarters. In vitro, an OVA-restimulation of PBMC or whole blood of sensitized cows induced the production of IL-17A and IFN-γ. The characterization of the IL-17A-producing leukocytes is underway. These results suggest that a Th17-type immune response can be induced in the MG by immunization to protein antigens, in parallel to a Th1-type response. As IL-17A is known to be involved in the immune defense against extracellular bacteria, and as we previously showed that bovine mammary epithelial cells respond to IL-17A by producing chemokines and antimicrobial peptides, we hypothesize that this cytokine contributes to the defense of the mammary gland against mastitis-causing bacteria.