Laziness

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occur in advancing lesions before the
accumulation of inflammatory cells. These changes are mediated by
activated CD4+ T lymphocytes and can be detected before visible pathology
to the skin occurs. Activated T lymphocytes exhibiting an increase in
HLA-DR and IL-2R can be seen in close proximity to Langerhans cells in the
dermis before lesion formation. Since Langerhans cells are antigen
presenting cells, activation of the T cells may occur by the recognition
of an as-yet unidentified antigen in the context of MHC class II. These
activated T lymphocytes then migrate to the epidermis and activate
epidermal keratinocytes.
At this point, a cascade of events occurs and appears to become
cyclic after up-regulation of certain cytokines. This cyclic tendency is
probably responsible for the static nature of many psoriatic plaques. An
increase in ICAM-1 and ELAM-1 (endothelial leukocyte adhesion molecule) in
the vascular endothelium underlying the plaque recruits ...

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Type I sufferers are positive for this HLA
haplotype. The correlation isn't as great for Type II sufferers - fifteen
percent - but is still significant. There is a lesser association with
other HLA haplotypes as well, notably A1, B13, B17, B27, B37, DR7, but
some of these may be due to linkage disequilibrium with Cw6. One study
showed that transgenic rats expressing haplotype B27 develop
psoriasis-like plaques on their tails, strengthening the argument for HLA
correlation. Furthermore, the most common cutaneous manifestation
associated with HLA-B27 is Reiter's syndrome (keratoderma blenorrhagica),
which shares clinical and histophysiological features with psoriasis.
There is ...

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