4.3 Article

Infection and thyroid autoimmunity: A seroepidemiologic study of TPOaAb

Journal

AUTOIMMUNITY
Volume 42, Issue 5, Pages 439-446

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.1080/08916930902787716

Keywords

Autoantibodies; seroepidemiology; thyroperoxidase; thyroiditis; T. gondii

Categories

Funding

  1. National Institute of Child Health
  2. Human Development
  3. NIH
  4. Stanley Division of Developmental Neurovirology
  5. JHMI
  6. NIHNational Institute of Mental Health/NIH [MH 070333, MH 53188]
  7. NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH053188, R03MH070333] Funding Source: NIH RePORTER

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Infectious agents have been implicated as triggers of autoimmunity. Prospective epidemiologic studies of infection with specific pathogens and the subsequent elevation of specific autoantibodies are difficult and costly to conduct. As a result, a solid body of evidence regarding this theoretically intriguing connection remains to be accrued. We studied term sera from 1807 pregnancies in 1591 women for whom IgG status for cytomegalovirus, Epstein-Barr virus, herpes simplex virus type 1, herpes simplex virus type 2, and/or Toxoplasma gondii was available from prior analyses. We tested the sera (masked regarding infectious status) for autoantibodies to thyroid peroxidase (TPOaAb) and then unmasked and linked them. Adjusted for other cofactors, prior infection with T. gondii was associated significantly with the elevation of TPOaAb, whereas seropositivity for other infections was not. Negative and positive findings for suspected triggers of autoimmunity should be reported to build the evidentiary basis needed to advance our understanding of the disease process. The positive association observed between prior infection with T. gondii and the elevation of TPOaAb is supported by an almost simultaneous study. These findings require further investigation. We believe that if T. gondii is in fact confirmed to trigger or enhance a TPOaAb response, the most likely mechanism involved is the bystander effect.

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