Final answer:
The pathogenesis of pemphigus involves autoantibodies against desmoglein proteins, leading to cell detachment and blister formation. T cells also contribute to inflammation and tissue damage.
Step-by-step explanation:
The pathogenesis of pemphigus involves the production of autoantibodies against desmoglein 1 and 3, which are proteins found in the desmosomes of epithelial cells. These autoantibodies bind to desmogleins and disrupt the normal connections between cells, leading to the detachment of cells from each other. This results in the formation of blisters on the skin and mucous membranes.
In addition to autoantibodies, T cells also play a role in the pathogenesis of pemphigus. T cells produce cytokines that contribute to the inflammation and tissue damage seen in pemphigus.