Psoriasis is a multi-factorial skin disease with a complex pathogenesis

Current concepts in the pathogenesis of psoriasis.
Das RP, Jain AK, Ramesh V.

Institute of Pathology (ICMR), Safdarjang Hospital and Vardhman
Mahavir Medical College, New Delhi, India.

Abstract
Psoriasis is a multi-factorial skin disease with a complex
pathogenesis. Various factors which have been suggested to play a key
role in the pathogenesis are T cells, antigen presenting cells
(APC's), keratinocytes, Langerhans' cells, macrophages, natural killer
cells, an array of Th1 type cytokines, certain growth factors like
vascular endothelial growth factor (VEGF), keratinocyte growth factor
(KGF), and others. It has been hypothesized that the disease starts
with the activation of T cell by an unknown antigen, which leads to
secretion of an array of cytokines by activated T cells, inflammatory
cells, and keratinocytes. The characteristic lesion of psoriasis is
due to the hyper-proliferation of the keratinocyte. Activated
Langerhans' cells migrate from skin to lymph nodes presenting the
antigen to nodal naïve T cells (cells that have not been activated by
antigen previously). The T cells activated by non-antigen-dependent
mechanism may, however, become antigen-specific memory cells that
react with a cross-reactive auto-antigen such as keratin (molecular
mimicry). The genetic background of the disease may be suggested from
the fact that concordance rate is 63-73% in monozygotic twins, as
compared to 17-20% in dizygotic twins. Several disease susceptibility
loci have been suggested as predisposing factors, PSORS1-PSORS9.