Behcet's disease is a chronic inflammatory disorder of unknown etiology. It
has long been postulated that immunological abnormalities, which are possi
bly induced by, microbial pathogens in genetically susceptible individuals,
are important in its pathogenesis. Recent findings have both supported the
significance of genetic factors and better defined the nature of inflammat
ion in Behcet's disease. Molecular genetic studies have strengthened the pr
imary association of HLA-B51 with Behcet's disease. The exact pathogenic me
chanism of the HLA-B51 molecule is still unknown, and its contribution to t
he overall genetic susceptibility to Behcet's disease is estimated to be le
ss than 20%. Spontaneous and/or induced overexpression of pro-inflammatory
cytokines (mainly Th1 type)from various cellular sources seems responsible
for the enhanced inflammatory reaction in Behcet's disease, and it may be a
ssociated with the genetic susceptibility . An antigen-driven immune respon
se superimposed on this primed-state and induced by heat shock proteins or
other peptides,from different strains of streptoccocci or other microbial a
gents has been suggested to trigger manifestations of Behcet's disease. End
othelial activation/injury and the resultant occlusive vasculopathy may als
o contribute to the tissue damage.