Pathogenesis
Hypersensitivity reactions are an overreaction of the immune system to an antigen which would not normally trigger an immune response.
The damage and clinical symptoms result from the body’s response to the substance rather than damage caused by the substance itself.
The vulnerability of an individual to these reactions can have a genetic link. Overreaction to innocuous antigens are linked to changes in the CD regions of T-helper cellmembranes, explaining why reactions like peanut allergies can commonly run in families. Overreaction to self-antigens is normally due to a failure in central tolerance, and this failure can also have genetically-inheritable features.
As is the case for many immune reactions, hypersensitivity reactions require two separate interactions of the immune system with the antigen.
The first time an antigen enters the body, it is picked up by antigen-presenting cells (such as macrophages or dendritic cells) and taken to the nearest lymph node, where it is presented to naïve T-cells. Cross-linking of the antigen with T-cells, as well as co-stimulatory molecules, can lead to activation of that T-cell and subsequent differentiation into “primed” Th1, Th2, or Th17 cells, which are specific to that antigen and can stimulate further immune responses if they meet the antigen again.
It is this second meeting that could result in a hypersensitivity reaction.