ABSTRACT

Behçet disease (BD) is a chronic, relapsing, systemic inflammatory disease. Although several immunological abnormalities have been demonstrated, the exact mechanism of the inflammatory changes occurring remains to be elucidated. The most probable hypothesis is that of an inflammatory reaction set off by infectious agents such as herpes simplex virus 1 or Streptococcus spp. or by an autoantigen such as heat schock proteins in genetically predisposed individuals.

Association of HLA-B51 is known as the strongest genetic susceptibility factor for BD. Recent genome-wide studies has confirmed this relationship, and reported new susceptibility genes (IL10, IL23R, IL12RB2, HLA-C*1602, HLA-C*1502 ve HLA-A*201) for the disease. Environmental factors, especially infectious agents (S. sangius etc.) are considered to play important roles in the development of BD. Current data suggest that high microbial load and associated stress proteins found in dental tissues and oral ulceration of patients with BD may iniate immunological crossreaction with the heat shock proteins (HSP) and subsequently the development of autoreactive T cells clones. This pathway may cause over expression of Th1 and Th17 type immune response. On the contrary, regulatory T cells response is suppressed. Th17 and IL-17 pathway are active in BD patients, and play an important role particularly in acute attacks of the disease.