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Infections May Have a Protective Role in the Etiopathogenesis of Celiac Disease
Author(s) -
Plot Leeor,
Amital Howard,
Barzilai Ori,
Ram Maya,
Nicola Bizzaro,
Shoenfeld Yehuda
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04814.x
Subject(s) - molecular mimicry , immunology , disease , cytomegalovirus , pathogenesis , treponema , rubella virus , immune system , virus , serology , rubella , virology , biology , medicine , antibody , syphilis , herpesviridae , viral disease , vaccination , measles , pathology , human immunodeficiency virus (hiv)
Infectious agents have been implicated in the pathogenesis of many autoimmune diseases via various pathogenic mechanisms, such as molecular mimicry, resulting in modulation of the host's immune tolerance. In the following article we examine the association between serological evidence of past infection with Toxoplasma gondii , rubella virus, cytomegalovirus, Treponema pallidum , and Epstein–Barr virus, and the co‐existence of celiac disease. Our results imply that certain infections may generate an immunological environment that disfavors future appearance of certain autoimmune conditions such as celiac disease.