Natural Antibodies Against Enteromicrobes and their Toxins for the Treatment of Rheumatoid Arthritis

Abstract

Autoimmune diseases (ADs) are thought to be brought on by the host immune system accidentally attacking and destroying its own tissue. “Molecular mimicry,” which asserts that antibodies against an infectious agent cross-react with a self-antigen possessing an identical or similar antigenic epitope, is a generally recognised theory to explain the pathogenic mechanism of ADs. This theory, however, was probably developed using false antibody assay data that was heavily impacted by strong false positive results in immunoassay equipment. Therefore, it is strongly recommended that this hypothesis be reevaluated using an adequate blocking agent capable of removing all sorts of nonspecific reactions and an acceptable assay design. In this review, we explore the notion that reduced immune function may be the fundamental, prevalent defect in ADs, increasing vulnerability to possible GI pathogens, such as bacteria and their components or food components, that may cause the disease. The host defensive system, which is carefully regulated by “immune function,” “mucosal barrier function,” and “intestinal bacterial balance,” may also be affected by abnormalities in the host's physical state. These disruptions may set off a chain reaction that can result in persistent health issues and eventually an autoimmune illness.