Chlamydial infections are among the most common human infections. Every year, in millions of humans, they cause infections of the eyes, the respiratory tract, the genital tract, joints, and the vasculature. Chlamydiae are obligate intracellular prokaryotic pathogens. Chlamydiae promote, in susceptible host cells that include mucosal epithelial cells, vascular endothelial cells, smooth muscle cells, and monocytes and macrophages, their survival while causing disease of varying clinical importance and consequence in their hosts. Chlamydia infections often precede the initiation of autoimmune diseases, and Chlamydiae are often found within autoimmune lesions. Thus, they have been suspected in the etiology and pathogenesis of autoimmune diseases. Autoimmune diseases have many causes. Genes, notably genes encoding cell-surface proteins that display peptides for immune recognition, the major histocompatibility complex (MHC), the environment, and the microbial diversity within the human body determine the susceptibility to autoimmune diseases. One mechanism by which infection is linked to the initiation of autoimmunity is termed molecular mimicry. Molecular mimicry describes the phenomenon of protein products from dissimilar genes sharing similar structures that elicit an immune response to both self and microbial proteins. Molecular mimicry might thus be a mechanism by which infections trigger autoimmune diseases. For the purpose of this chapter, we will focus on chlamydial proteins that mimic host self-proteins and thus contribute to initiation and maintenance of autoimmune diseases. Thus far, the strongest cases for molecular mimicry seem to have been made for chlamydial heat shock proteins 60, the DNA primase of Chlamydia trachomatis, and chlamydial OmcB proteins.