198282
Pemphigus
pathophysiology
- Autoantibodies inhibit adhesive fn of Dsg and lead to loss of cell-cell adhesion of keratinocytes causing blisters
- IgG autoantobodies against Dsg1 and Dsg3 are pathogenic
and have 1ry role in blister formation
- serum anti-Dsg1 and 3 autoantibodies measured by IIF or ELISA correlate with dz severity
- IgG from PV sera w extracell domain of
Dsg3 causes suprabasilar acantholysis
when injected into neonatal mice
- After immunoabsorption of
anti-Dsg3, serum no longer
produces blisters
- After immunoabsorption of
anti-Dsg3, serum no longer
produces blisters
- Immunoabsorption of PF sera with extra cell domains of Dsg1 eliminates pathogenic activity.
- IgG from patient's sera can cause superfine blisters in
neonatal mice
- IgG from patient's sera can cause superfine blisters in
neonatal mice
- Monoclonal Abys against Dsg from a
mouse model of pemphigus and from
human patients induce blisters
histology similar to those in patients
with naturally occurring dz
- serum anti-Dsg1 and 3 autoantibodies measured by IIF or ELISA correlate with dz severity
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