The continuum of clinical phenotype between different autoimmune thyroid diseases and mainly the common pathophysiological mechanisms have lead to a novel classification of these disorders into three types: (1) Type 1 autoimmune thyroiditis (euthyroidism associated with the presence of anti-thyroglobulin and anti-thyroperoxydase autoantibodies); (2) Type 2 autoimmune thyroiditis or Hashimoto's disease (hypothyroidism with anti-thyroglobulin and anti-thyroperoxydase autoantibodies). Postpartum thyroiditis falls into this category and is characterized by transient hyperthyroidism followed by hypothyroidism; and (3) Type 3 autoimmune thyroiditis or Graves-Basedow's disease (hyperthyroidism with anti-TSH receptor "stimulating" auto-antibodies, often associated with anti-thyroglobulin and anti-thyroperoxydase autoantibodies). Thyroid orbitopathy often complicates Type 3 autoimmune thyroiditis and is thought to result from an autoimmune response against an autoantigen common to thyroid and orbital fibroblasts/adipose cells. We present the actualized knowledge about the immunological parameters that can be detected and quantified in autoimmune thyroid diseases, about the pathophysiological mechanisms involved in these disorders, and about the options of their treatment that are currently offered to the medical community.