Table 1 Theoretical reasons why type 3 immunity should contribute to MG defense against pathogens.
From: Type 3 immunity: a perspective for the defense of the mammary gland against infections
Features of type 3 immunity | Features of mammary gland defenses | Ref |
|---|---|---|
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 | |
Signature cytokines: IL-17A, IL-17F, IL-22 | IL-17A, IL-17F, IL-22 in mastitic milk | |
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] |