Since the discovery of immunologic tolerance phenomenon, active discussion of the role of genetic and environmental factors in autoimmune disease development has persisted. One of such factors is infections. Microorganisms are considered to be triggers of autoimmune diseases but their role is still not completely understood. Animal experiments conclusively demonstrate how the certain microorganism or its antigen can cause autoimmune pathology. At the same time the results of clinical studies performed on patients with different autoimmune pathologies are hardly decisive and often are contradictory. It should be taken into account that patients with already existing disease were studied in most cases, so interpretation of the data on the association of certain causative pathogens with certain autoimmune pathology should be performed cautiously. The review contains key hypotheses about possible mechanisms of autoimmune reaction development in infections: hypotheses about latent antegens/cryptoantigens, antigen modification, superantigen presence, epitope spectrum extension, molecular mimicry, adjuvant and non-specific effect, antigen complementarity, and idiotypic-antiidiotypic interactions. Their advantages and disadvantages are presented, their comparison is performed. In most cases facts proving one of the hypotheses can be reconsidered in favor of another one. A number of early hypotheses need to be reviewed taking into account modern understanding of innate and adaptive immunity. As more data about relation between infection and autoimmunity is collected, new hypotheses can be developed integrating main claims of previous hypotheses and adding the new ones.