Psoriasis

There is considerable evidence that T lymphocytes play an important role in development of

plaques of psoriasis. This includes: (i) early infl ux of T cells into expanding lesions [39,40];
(ii) strong association with the MHC, particularly HLA-Cw6 [41]; (iii) ablative (albeit
temporary) effect of anti-T-cell therapy [42]; (iv) increased antigen presentation in psoriatic
plaques [43]; (v)

Further, in psoriatic stratum corneum, there is an abundance of antimicrobial peptides such as

defensins and cathelicidins, which have the capacity to activate innate immunity.

Innate immune mechanisms in turn lead to antigen driven Tcell expansion and activation. The
key question remains as to the nature of the antigen involved. To date this is unresolved but
evidence of an antigen-specifi c response includes: (i) limited clonality of infi ltrating T cells;
(ii) persistence of T-cell clones in plaques over several years; and (iii) identical T-cell clones
in tonsils and skin of patients with Streptococcus-associated psoriasis [48]. Historically,
evidence has suggested a primary role for Th1-type response in disease pathogenesis.
However, it has recently been established that a more recently described subset of T cell,
thought to play a key role in autoimmunity, termed Th17, is the primary pathogenic subset.
Evidence includes genetic association (see above), with IL-23 being a key cytokine in
generation of Th17 cells, abundance of IL-23 in psoriatic tissue [49] and induction of a
psoriatic phenotype by IL-23 in animal models [50]. Other cytokines downstream of IL-23 in
Th17 pathways, including IL-17 and IL-22, have similar functional effects.

Based on the above information, a pathogenic model has been suggested in which aberrations
in the stratum corneum trigger activation of innate immune mechanisms, which in turn lead
to recruitment and activation of Th17 cells, which provide effector cytokines leading to
epidermal hyperproliferation and a proinflammatory state [3]. Such mechanisms provide a
scientifi cration ale for the use of biological therapies

Treatment

Tar preparations and vitamin D analogues are appropriate, but corticosteroids can be used for
localized psoriasis. If necessary, dithranol can be introduced later
but is more diffi cult to handle. If sunlight or UVB phototherapy
are available, light can be added at this stage or earlier. Special
routines may be necessary for the scalp. If the psoriasis is severe
and extensive and the above initial measures have failed, more
intensive tar or dithranol therapy should be considered, in a daycare
unit or a hospital if such facilities exist, with or without UV
phototherapy.