Table 1.

Major advantages and disadvantages of individual BD models.

Model	Major Advantage	Major Disadvantage
HLA-B*51 [55]	Transgenic mouse model developed being gene associated with BD	No clinical BD symptoms
Alpha-tropomyosin [66]	Model developed using antibodies found in BD patients	Alpha-tropomyosin antibody only found in a small subset of BD patients
Heat shock protein [94]	Models involvement of a protein that has already been shown to be associated with BD	No significant differences in the mRNA levels of Th1 and Th2 cytokines in immunized animals vs. those that were not immunized.
S antigen (S-Ag) [107] [105]	Successfully induced EAU in guinea pigs with increased superoxide production (uveitis and increased superoxide production have been observed with BD patients) EAU also successfully induced in Lewis rats immunized with both S-Ag and Hepatitis B virus peptides implying autoreactive mechanisms activated by a viral infection	May not be useful for more comprehensive studies.
Human sera [110]	Model developed using antibodies found in BD patients	Sera possibly containing heterogeneous mixture of antibodies against different targets and not actual antigens were used; therefore, one cannot be certain that changes observed were induced solely or even partly by antibodies against neuropil antigens.
Herpes simplex virus type 1 [116]	Best able to recapitulate BD phenotype	Low penetrance rates necessitate the use of large numbers of animals.