Immunity to extracellular bacteria and fungi |
Infection by extracellular bacteria |
[61] |
Defense of epithelial barriers |
Mainly epithelial infection (“duct disease”) |
[62] |
Amplifies neutrophilic inflammation |
Neutrophils main cell type recruited during mastitis |
[63] |
Neutrophils important effector arm of type 3 immunity |
Neutrophils main immune defense of the mammary gland |
[63] |
Induces epithelial self-defense by antimicrobial peptides |
Mammary epithelial cells produce AMPs in response to bacteria or cytokines |
[62] |
Targets epithelial cells to trigger inflammation (chemokines) |
Mammary epithelial cells respond to IL-17A by secreting chemokines |
[17, 24] |
Signature cytokines: IL-17A, IL-17F, IL-22 |
IL-17A, IL-17F, IL-22 in mastitic milk |
[19, 23] |
Targets epithelial cells through receptors to IL-17 and IL-22 |
Mammary epithelial cells express IL-17R and respond to IL-17A & IL-17F |
[24] |
Immunization elicits CD4 + cells producing IL-17 (Th17 lymphocytes) |
CD4 + IL-17A + cells correlate with vaccination or antigen-specific sensitization of the mammary gland |
[33] |
The IL-23/IL-17 axis drives granulopoiesis |
Mastitis drains neutrophil reserves |
[64] |