Molecular Mimicry and Its Effect on Crohn's Disease

Abstract or Introduction

Molecular mimicry is a well-documented biological phenomenon and its link to autoimmune diseases has led to extensive research. From an epidemiological perspective, autoimmune diseases have been found to exhibit multifactorial origins. In most cases, genetic predisposition, as well as environmental factors leads to tissue injury owing to the activity of autoreactive antibodies or T cells. One of the most striking characteristics of autoimmune diseases is that the initial biological processes that lead to the loss of tolerance do not match with clinical manifestations. These manifestations occur long after the mechanisms associated with loss of tolerance. It is believed that loss of tolerance is responsible for the severity of chronic autoimmune diseases. Currently, there are several pathological processes involved in the breakdown of immunologic tolerance. These mechanisms include activation of polyclonal lymphocytes, abnormalities in self antigens presentation, molecular mimicry, and presence of autoreative lymphocytes (Bellone, 2005). In Crohn’s disease, as well as other autoimmune diseases such as ulcerative colitis, multiple sclerosis, and type 1 diabetes mellitus, molecular mimicry is hypothesized to be one of the key mechanisms leading to the breakdown of immunological self tolerance. Therefore, this paper will provide a comprehensive overview on molecular mimicry and its effects on autoimmune diseases with a principal focus on Crohn’s disease.