Moudgil, K.D., Chang, T.T., Eradat, H., et al. (1997) Diversification of T cell responses to carboxy-terminal determinants within the 65 kD heat-shock protein is involved in regulation of autoimmune arthritis. Journal of Experimental Medicine, 185, 1307-1316. doi:10.1084/jem.185.7.1307

has been cited by the following article:

• TITLE: Mycobacterium avium subspecies paratuberculosis—An environmental trigger of type 1 diabetes mellitus

  AUTHORS: Coad Thomas Dow

  KEYWORDS: Autoimmune Diabetes; T1DM; Paratuberculosis; MAP; HSP65; Molecular Mimicry

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.2 No.1, February 22, 2012

  ABSTRACT: Type 1 diabetes mellitus (T1DM) is an autoimmune disease. The etiology of T1DM is incompletely understood but environmental agent(s) are thought to trigger T1DM in the genetically at-risk. Humans are widely exposed to Mycobacterium avium subspecies paratuberculosis (MAP), a proven multi-host chronic enteric pathogen that is mostly studied in ruminant animals and causes the inflammatory disease paratuberculosis or Johne’s disease. In humans, MAP is the putative cause of Crohn’s disease and has been linked to sarcoidosis, autoimmune thyroiditis, multiple sclerosis and autoimmune diabetes. The role of MAP as a trigger for T1DM was first postulated in 2005; subsequent studies suggest a link. This article discusses MAP, human exposure to MAP, genetic susceptibility to MAP and MAP in human disease including T1DM.