Some pathogen
infections and immune system deficiencies have been linked to a few
autoimmune diseases. However, the pathogenesis of most
autoimmune diseases is unknown. An explanatory hypothesis for the pathogenesis of
infection-initiated
autoimmune diseases is provided. Virulent pathogen
infections create extensive pathogen
antigens that frequently require
antibodies. These
antibodies create extensive
antigen-antibody
immune complexes, which some immuno-compromised individuals will not adequately eliminate. This will cause inflammatory
type III hypersensitivity symptoms, including
protease releases that destroy epithelium, mesothelium and endothelium basement membranes, express new immunogenic
antigens from previously sequestered basement membrane constituents, and ultimately induce new
autoantibodies. This can continue after the
infection ends, if the first wave of
protease attacks on basement membranes induces new
autoantibodies that cause new uncleared
antigen-antibody
immune complexes and
type III hypersensitivity reactions. The secreted
proteases and other
enzymes will have preferred substrates and these
proteases or other
enzymes by themselves, or by their processed
protein substrates, can express immunogenic
antigens that induce new
autoantibodies and initiate various
autoimmune diseases. In summary, several
autoimmune diseases can be initiated in immuno-compromised individuals during extensive pathogen
infections, if these individuals have two immune problems: (a) slow or weak initial immune responses that result in a reliance on
antibodies and (b) an inability to eliminate the resulting
antigen-antibody
immune complexes by phagocytosis. These two immune problems and the resulting immune system
type III hypersensitivity reaction can explain the causation of several
autoimmune diseases, including the most common and the rarest
autoimmune diseases, both their differences and their similarities.