Hakaru Hashimoto described 4 patients with a hitherto unknown cause for goitre, 
struma lymphomatosa, a century ago. He was careful to distinguish this from 
Riedel thyroiditis but it has become clear that fibrosis and atrophy of the 
thyroid are indeed components of Hashimoto thyroiditis, and in rare cases 
IgG4-related sclerosing disease may be an outcome. Although the cause of the 
lymphocytic infiltration was unknown to Hashimoto, we now know through the 
pioneering studies of N.R. Rose and E. Witebsky [J Immunol 1956;76:417-427] that 
this condition is the archetype for autoimmune destruction as a disease 
mechanism. In the last two decades in particular, there has been huge interest 
in unravelling the genetic basis for this and related autoimmune disorders. The 
list of polymorphisms associated with autoimmune thyroid disease grows each 
year, and in the case of vitiligo, which is frequently found in association with 
thyroid autoimmunity, we know that 27 separate susceptibility loci account for 
less than 20% of the heritability of this condition. Environmental and 
existential factors may turn out to be just as complex in number and in 
interactions. We can thus imagine a 'Swiss cheese' model for the causation of 
autoimmune thyroid disease, in which the effects of cumulative weaknesses line 
up - like the holes in slices of cheese - to allow the catastrophic event of 
autoimmune destruction to occur.