The Immunopathology of Psoriasis

Abstract

Psoriasis affects approximately 2% of the population in Western countries. Although clinically rather monomorphic, the disease presents with a number of phenotypically distinct and heterogeneous subgroups showing differences in their pathogenetic pathways. Patients with type I (early onset) psoriasis demonstrate inflammatory lesions with epidermal hyperproliferation and the presence of activated T cells as well as intraepidermal polymorphs as principal features. In contrast to pustular types of psoriasis, these patients show genetic susceptibility and strong association with MHC class I and class-I haplotypes. There is evidence for a T-cell-mediated pathomechanism leading to a large spectrum of regulatory mediators including cytokines and growth factors as well as lipid mediators which are abnormally expressed. Pathogenetically psoriasis shows features in common with chronic relapsing T-cell-mediated diseases including Crohn’s disease, rheumatoid arthritis and others.

Histopathologic diagnostic parameters of psoriasis; a clinicopathological study

“…Because of the rapid keratinocyte proliferation, there is aberrant retention of intact nuclei in the terminally differentiated keratinocytes resulting in parakeratosis and paucity of granular layer, which can vary from hypogranulosis to agranulosis. [20][21][22] This mechanism of defective keratinocyte proliferation also explains the presence of parakeratosis and irregular acanthosis in all the cases of psoriasis encountered in our study.…”

The Serum Levels of Malondialdehyde, Vitamin E and Erythrocyte Catalase Activity in Psoriasis Patients

“…During subsequent development neutrophils began to appear between the upper layers forming pockets (Micro-abscesses). Neutrophil migration into the epidermis was most pronounced in active disease and occurred in a rhythmic pattern [25].…”

993 CARD14 gain-of-function mutation alone is sufficient to drive IL-23/IL-17-mediated psoriasiform skin inflammation in vivo

“…The etiology of psoriasis has been elusive in the past, regarding the contribution of keratinocyte dysfunction versus altered immune function (Bos et al, 2005;Christophers, 1996). However, our data strongly suggest that dysregulated keratinocyte signaling pathways initiated by CARD14 contribute to drive the pathogenic IL-23/IL-17 axis in vivo.…”