Fas  (Apo-1/CD95)   ts  a widely  expressed mem brane-anchored    protein   that  induces   apoptosis. Keratinocytes   constitutively    express 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 re ceptor.  It  can  antagonize   cell  surface  Fas func tion  by  downregulating   Fas-mediated    apoptosis and    its    level    may    be    regulated     by    pro inflammatory  cytokines.   Therefore,   the  purpose of this study  was 10  investigate   the role of apoptotic   inhibitors,   slias  and  Bcl-Z  (B-cell   lvmphoma

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 -2),  and  pro-inflammatory    cytokine,   interleukin-6  (IL-6),   in patients   with  psoriasis   vulgaris and  their possible   correlations   to disease  activitv. Sera from fiftv patients   with psoriasis   vulgaris and  20  healthy   controls   were  tested  for  slias. Bcl-2  and  IL-6   levels  using  ELISA   assays.  According  to disease  activity,   psoriasis  area severity index  (PASI  score),   the patients   were  classified   info   mild   (11=3 I),     moderate    (n= 11)    and severe  (11=8)  cases.  Serum  levels  of  slias. 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.  In conclusion,    these   results   suggest    that   the   psoriasis vulgaris   was  associated    with  increased   serum levels  of slias,  Bcl-2 and  IL-6   .   This  may  explain two  major pathological   features  in psoriasis:   ep idermal   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   of  !L-6.  The  lack  of  correlation   between  sFas  c111d  Bcl-2 could  be attributed   to their different  mechanisms   of anti-apoptotic    actions.