IntroductionF: as (Apo-I /CD95)  is a widely  expressed  membrane-anchored   protein that induces apoptosis.  Keratinocytes  constitutively   express  the Fas antigen  and Fas- mediated  apoptosis  may characterize  several  pathological  conditions  affecting  human skin.  Soluble Fas (sFas) has been demonstrated   in serum by alternative  mRNA  splicing of Fas receptor.  It can antagonize  cell surface Fas function  by downregulating   Fas- mediated  apoptosis  and its level  may be regulated  by pro-inflammatory   cytokines.

Rationale:  The purpose  of this study was to investigate  the role of apoptotic  inhibitors, sFas and Bcl-2 (B-cell lymphoma-2),  and pro-inflammatory   cytokine,  interleukin-6   (IL-6), in patients  with psoriasis  vulgaris  and their possible  correlations  to disease  activity.

Methods: Sera from fifty patients  with psoriasis  vulgaris  and twenty healthy  controls were tested for sFas, Bcl-2,  and IL-6 levels using ELISA  assays.  According  to disease activity,  psoriasis  area severity  index (PASI score), the patients  were classified  into mild (n=31), moderate  (n=l 1) and severe  (n=8) cases.

Results: Serum levels of sFas, Bcl-2 and IL-6 were significantly  higher  in patients  than controls.  Serum  levels of sFas and IL-6 in severe cases were significantly  higher than mild and moderate  cases. Significant  positive  correlation  between  PASI score and both sFas and IL-6 and between  IL-6 and sFas were shown. However,  no significant correlation  was observed  between  Bcl-2 and both sFas and IL-6.

Conclusions: Psoriasis  vulgaris  was associated  with increased  serum levels of sFas, Bcl-2 and IL-6. This may explain two major pathological   features  in psoriasis;

epidermal  hyperplasia  and inflammation.  Therefore,  we support  the possibility  of a role of sFas in the pathogenesis   of psoriasis  by downregulating   Fas mediated  apoptosis  and thus potentiating  the action  ofIL-6.  The lack of correlation  between  sFas and the Bcl-2 could be attributed  to their different  mechanisms  of anti-apoptotic   actions.