Front Immunol. 2015 Mar 04;6:96. doi: 10.3389/fimmu.2015.00096. eCollection 2015.
Frontiers in immunology
Leonardo A Sechi, Coad Thomas Dow
PMID: 25788897 PMCID: PMC4349160 DOI: 10.3389/fimmu.2015.00096
The factitive role of Mycobacterium avium ss. paratuberculosis (MAP) in Crohn's disease has been debated for more than a century. The controversy is due to the fact that Crohn's disease is so similar to a disease of MAP-infected ruminant animals, Johne's disease; and, though MAP can be readily detected in the infected ruminants, it is much more difficult to detect in humans. Molecular techniques that can detect MAP in pathologic Crohn's specimens as well as dedicated specialty labs successful in culturing MAP from Crohn's patients have provided strong argument for MAP's role in Crohn's disease. Perhaps more incriminating for MAP as a zoonotic agent is the increasing number of diseases with which MAP has been related: Blau syndrome, type 1 diabetes, Hashimoto thyroiditis, and multiple sclerosis. In this article, we debate about genetic susceptibility to mycobacterial infection and human exposure to MAP; moreover, it suggests that molecular mimicry between protein epitopes of MAP and human proteins is a likely bridge between infection and these autoimmune disorders.
Keywords: Crohn’s; MAP; autoimmune; autoimmune thyroiditis; molecular mimicry; multiple sclerosis; paratuberculosis; type 1 diabetes