Bacterial molecular mimicry in autoimmune diseases

Bacterial molecular mimicry in autoimmune diseases is one of the leading mechanisms by which microorganisms may induce autoimmunity and survive in the host. The main purpose of the current study was to determine the main microbes that elicit autoimmune reactions through molecular mimicry and identify the most relevant approaches to investigate this mechanism. A classic example is the M protein of Streptococcus pyogenes, which induces antibody cross-reactivity with a cardiac protein and causes rheumatic fever. Another notable example is the protein from Porphyromonas gingivalis that closely resembles the human heat shock protein and accelerates atherosclerotic. There is evidence that antibodies against Helicobacter pylori CagA interact with different parts of smooth muscle and endothelial cells enhancing atherosclerotic vascular disease. Recently, one cause of infertility has been associated with Staphylococcus aureus molecular mimicry that triggers an antibody response that cross-reacts with human spermatozoa proteins. Further examples of bacterial molecular mimicry are associated with Chlamydia pneumoniae, Escherichia coli, Yersinia, and Salmonella. From the literature, the most widely used methods in this field are Basic Local Alignment Search Tool (BLAST), serological assays, and phage display. The subjects of particular concern are vaccine cross-reactivity and immunosuppressive drugs side-effects, therefore alternative approaches are needed. Such an approach is phage display where therapeutic antibody fragments obtained by this technique have been used in the treatment of autoimmune diseases by neutralizing the pathological effects of autoantibodies. Phage display libraries are constructed from the antibody repertoires of autoimmune disease patients. Antibody fragments without the Fc domain can not interact with Fc receptors and proteins of the complement system and trigger autoimmune diseases. Another approach is to block the Fc receptors.  In conclusion, this review highlights key aspects of bacterial molecular mimicry to better understand the factors associated with autoimmune diseases and encourage further research in this field.