Immunological and autoimmune manifestations are often associated with Borrelia infection. These include autoantibody production with production of antinuclear antibodies and rheumatoid factors 15, 16, anti‐myelin 17 and antiganglioside antibodies 18 associated molecular mimicry against the myelin sheath surrounding nerves leading to demyelination 19, and production of inflammatory mediators including chemokines
Another factor which plays a role in Borrelia's pathogenesis is the bacteria's ability to suppress long‐lived humoral immunity. Deficiencies of cellular and humoral immunity during Borrelia infection had been previously noted in the scientific literature 42 as antibodies often waned after infection with a prolonged IgM response 43 Baumgarth and colleagues recently reported that Borrelia burgdorferi rapidly targets lymph nodes and adversely affects germinal centers, which are required for the development of long‐lived plasma cells and continuous antibody secretion 44. Low IgG levels and subclasses may subsequently result, impairing the ability to effectively treat Lyme and associated bacterial infections.