Pathogen-Associated Autoimmunity

Treating EBV is presented as potentially reducing autoimmune antibody burden in lupus patients. Pathogen-triggered immune activation can produce antibodies that crossreact with human tissue through molecular mimicry. Pathogens are described as driving autoimmunity through antigen release and gut barrier disruption. Chlamydia antibodies are described as crossreacting with myelin basic protein and MOG, which are relevant to multiple sclerosis pathology. EBV is presented as crossreacting with lupus-associated antigens at about 70–80% structural homology. The diagnostic goal is to identify pathogens whose antibodies structurally crossreact with human tissue, not only to confirm active infection. Mold antibodies can identify both exposure or colonization and crossreactivity with cochlin in the inner ear.