Certain patients with silicosis have been reported to exhibit immunological
abnormalities such as the appearance of antinuclear antibodies and the occ
urrence of autoimmune diseases. Fas ligand (FasL) is a type II membrane pro
tein which induces apoptosis by binding to its membrane receptor, Fas. FasL
is converted to a soluble form by a metalloproteinase-like enzyme. We have
already found serum soluble Fas (sFas) levels in silicosis patients as wel
l as in patients with systemic lupus erythematosus (SLE) to be significantl
y higher than those in healthy volunteers. To examine further the role of t
he Fas/FasL system in silica-induced immunological abnormalities, we invest
igated serum soluble FasL (sFasL) levels in silicosis patients with no clin
ical symptoms of autoimmune diseases, using ELISA for sFasL. Although the s
erum sFasL levels in patients with SLE were significantly higher than those
in healthy volunteers and showed a slight positive correlation with serum
sFas levels, those in silicosis patients exhibited no significant differenc
e from those in healthy volunteers, and there was no correlation with serum
sFas levels. However, sFasL levels were elevated in silicosis patients wit
h slight dyspnoea or normal PCO2 among various clinical parameters of silic
osis. It may be speculated that the immunological disturbances presented by
the abnormalities of apoptosis-related molecules in silicosis patients do
not occur with a similar degree of respiratory involvement. Further studies
are required to clarify which kinds of factors are involved in silicosis p
atients who exhibit immunological abnormalities.