The keratinization process in
psoriasis is a unique phenomenon. We have proposed an organized system for keratinization in
psoriasis based on the recognition of early and late
differentiation markers combined with premature cell death. The early
differentiation markers, such as
involucrin, small
proline-rich
proteins (SPRR),
cystatin A and
transglutaminase l, are more conspicuously expressed in
psoriasis, while the late
differentiation markers, such as
profilaggrin and
loricrin, are abolished. Keratinization markers that are not observed in the normal epidermis are also detected; these include SKALP/
elafin as well as K6 and K16. With a markedly diminished turnover time, the psoriatic epidermis rapidly synthesizes
differentiation markers that are mostly under the control of the
protein kinase C-AP1 transcriptional control system. Because of the premature cell death, however, the late
differentiation markers are not expressed. During the improvement of the lesion and the therefore longer turnover time, the late
differentiation markers rapidly catch up to reveal their expression. This explains the rapid appearance of
keratohyalin granules (
profilaggrin) in the healing lesion of
psoriasis. Thus the keratinization process in
psoriasis can be explained by the accelerated keratinization combined with premature cell death. The keratinization process in
psoriasis is unique, because both accelerated keratinization and premature cell death co-exist, resulting in the disappearance of late
differentiation markers such as
profilaggrin and
loricrin. It is interesting to note that the premature cell death is also under the control of
protein kinase C signaling.