Molecular mimicry vs Epitope spreading Flashcards
describe several mechanisms involved in the development of autoimmune responses following microbial infection
Molecular Mimicry:
Description: Molecular mimicry involves the activation of cross-reactive TH1 cells that recognize both microbial epitopes (mTH1) and self epitopes (sTH1).
Process: Crossreactive T cells are activated, releasing cytokines and chemokines that recruit and activate monocytes and macrophages. This immune response can result in self-tissue damage.
Consequence: The release of self-tissue antigens perpetuates the autoimmune disease as these antigens are taken up by antigen-presenting cells (APCs).
Epitope Spreading:
Description: Epitope spreading occurs with a persistent microbial infection that activates microorganism-specific TH1 cells, leading to self-tissue damage.
Process: Self peptides are released during tissue damage, taken up by APCs, and presented to self-reactive TH1 cells. This continual damage and release of self peptides contribute to the spread of the self-reactive immune response to multiple self-epitopes.
Bystander Activation:
Description: Bystander activation is the nonspecific activation of self-reactive TH1 cells.
Process: Activation of microorganism-specific TH1 cells leads to inflammation, increased T cell infiltration at the site of infection, and activation of self-reactive TH1 cells by T-cell receptor (TCR)-dependent and -independent mechanisms.
Consequence: Self-reactive T cells activated in this manner mediate self-tissue damage and perpetuate the autoimmune response.
Cryptic Antigen Model:
Description: The cryptic antigen model describes the initiation of autoimmunity by the differential processing of self peptides.
Process: IFN-γ is secreted by both activated microbe-specific TH1 cells and microbe-infected tissue cells, activating APCs. APCs engulf self-antigens, and cytokine activation induces increased protease production and different processing of captured self-antigens.
Consequence: The presentation of cryptic epitopes can activate self-reactive TH1 cells, leading to self-tissue destruction.
