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M. paratuberculosis Heat Shock Protein 65 and Human Diseases: Bridging Infection and Autoimmunity

Coad Thomas Dow1

  • 1Chippewa Valley Eye Clinic, Wisconsin and Eye Research Institute, University of Wisconsin-Madison, 2715 Damon Street, Eau Claire, WI 54701, USA.

Autoimmune Diseases
|October 12, 2012
PubMed

Insights

Mycobacterium avium subspecies paratuberculosis (MAP) may trigger autoimmune diseases like type 1 diabetes and multiple sclerosis. This occurs through molecular mimicry involving its heat shock protein 65 (HSP65), which resembles human proteins.

Area of Science:

  • Microbiology
  • Immunology
  • Autoimmune Diseases

Background:

  • Mycobacterium avium subspecies paratuberculosis (MAP) causes Johne's disease in animals and is implicated in human Crohn's disease and sarcoidosis.
  • MAP has been recently associated with Blau syndrome, autoimmune diabetes, autoimmune thyroiditis, and multiple sclerosis.
  • The role of MAP in autoimmune diseases where autoantibodies are prominent is less understood.

Purpose of the Study:

  • To propose a mechanism by which MAP may trigger autoimmune diseases.
  • To investigate the role of mycobacterial heat shock protein 65 (HSP65) in molecular mimicry leading to autoantibody production.

Main Methods:

  • Review of existing literature on MAP, Johne's disease, Crohn's disease, sarcoidosis, and autoimmune conditions.
  • Analysis of the structural similarities between mycobacterial HSP65 and human host proteins.

Main Results:

  • MAP's heat shock protein 65 (HSP65) shares structural similarities with human proteins.
  • This molecular mimicry is hypothesized to stimulate the production of autoantibodies.

Conclusions:

  • MAP, through its HSP65, may act as a trigger for autoimmune diseases including type 1 diabetes, Hashimoto's thyroiditis, and multiple sclerosis.
  • The proposed mechanism involves molecular mimicry between MAP HSP65 and host proteins, leading to autoantibody generation.

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