Additionally, certain strains of T. gondii can secrete a protein known as GRA15, activating the NF-κB pathway, which upregulates the pro-inflammatory cytokine IL-12 in the early immune response, possibly leading to the parasites latent phase. The parasites ability to secrete these proteins depends on its genotype and affects its virulence.The parasite also influences an anti-apoptotic mechanism, allowing the infected host cells to persist and replicate. One method of apoptosis resistance is by disrupting pro-apoptosis effector proteins, such as BAX and BAK. To disrupt these proteins, T. gondii causes conformational changes to the proteins, which prevent the proteins from being transported to various cellular compartments where they initiate apoptosis events. T. gondii does not, however, cause downregulation of the pro-apoptosis effector proteins.T. gondii also has the ability to initiate autophagy of the hosts cells. This leads to a decrease in healthy, uninfected cells, and consequently fewer host cells to attack the infected cells. Research by Wang et al finds that infected cells lead to higher levels of autophagosomes in normal and infected cells. Their research reveals that T. gondii causes host cell autophagy using a calcium-dependent pathway. Another study suggests that the parasite can directly affect calcium being released from calcium stores, which are important for the signalling processes of cells.The mechanisms above allow T. gondii to persist in a host.
Pemphigus foliaceus is an autoimmune blistering disease (bullous disorder) of the skin. Pemphigus foliaceus causes a characteristic inflammatory attack at the subcorneal layer of epidermis, which results in skin lesions that are scaly or crusted erosions with an erythematous (red) base. Mucosal involvement is absent even with widespread disease.If there is an autoimmune IgG buildup in the epidermis, then nearly all of the antibodies are aimed against desmoglein 1. The effect of the antibodies and the immunological pathway is most likely one of three mechanisms:

Steric hindrance of the desmoglein 1: The antibody caps off the site for intracellular binding to another keratinocyte. Activation of an endocytic pathway: The antibody activates a pathway which causes an internalization of desmogleïn 1, which in turn causes a loss of adhesion. Disruption of function: In this case, the antibody blocks the desmoglein 1 from being formed into a desmosome. This in turn causes a loss of adhesion with acantholysis as a result. Cause
The National Institute of Arthritis and Musculoskeletal and Skin Diseases describes it like this:
Normally, our immune system produces antibodies that attack viruses and harmful bacteria to keep us healthy. In people with pemphigus, however, the immune system mistakenly attacks the cells in the epidermis, or top layer of the skin, and the mucous membranes. The immune system produces antibodies against proteins in the skin known as desmogleins. These proteins form the glue that keeps skin cells attached and the skin intact.