Molecular mimicry is one of the leading mechanisms by which infectious or chemical agents may induce autoimmunity.It occurs when similarities between foreign and self-peptides favor an activation of autoreactive Tor B cells by a foreign-derived antigen in a susceptible individual. However, molecular mimicry is unlikely to bethe only underlying mechanism for autoimmune responses; other factors such as breach in central tolerance,non-specific bystander activation, or persistent antigenic stimuli (amongst others) may also contribute to thedevelopment of autoimmune diseases. Host genetics, exposure to microbiota and environmental chemicals areadditional links to our understanding of molecular mimicry. Our current knowledge of the detailed mechanismsof molecular mimicry is limited by the issues of prolonged periods of latency before the appearance of disease,the lack of enough statistical power in epidemiological studies, the limitations of the potential role of genetics inhuman studies, the relevance of inbred murine models to the diverse human population and especially thelimited technology to systematically dissect the human T-cell repertoire and B-cell responses. Nevertheless,studies on the role of autoreactive T-cells that are generated secondary to molecular mimicry, the diversity of theT-cell receptor repertoires of auto-reactive T-cells, the role of exposure to cryptic antigens, the generation ofautoimmune B-cell responses, the interaction of microbiota and chemical adjuvants with the host immunesystems all provide clues in advancing our understanding of the molecular mechanisms involved in the evolvingconcept of molecular mimicry and also may potentially aid in the prevention and treatment of autoimmunediseases.