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Can Virus Infections Trigger Autoimmune Disease?

https://doi.org/10.1006/jaut.2000.0484Get rights and content

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  • Cited by (37)

    • Rotavirus and autoimmunity

      2020, Journal of Infection
      Citation Excerpt :

      Sex bias might be originated by differential sex hormones, fetal microchimerism or skewed X chromosome inactivation.22 Infectious pathogens including viruses and bacteria are considered the main environmental triggers,23–25 while changes in the intestinal virome precede the development of autoimmunity.26 Four mechanisms have been proposed to explain how pathogen infection can lead to autoimmunity: molecular mimicry, bystander activation, epitope spreading, and cryptic antigens.

    • Study of CD4<sup>+</sup>, CD8<sup>+</sup>, and natural killer cells (CD16<sup>+</sup>, CD56<sup>+</sup>) in children with immune thrombocytopenic purpura

      2017, Hematology/ Oncology and Stem Cell Therapy
      Citation Excerpt :

      It is not clear whether the NK cell alterations occur as a result of the disease or are involved in its pathogenesis [30]. Viral infections have been implicated in the pathogenesis of several autoimmune diseases due to molecular mimicry or polyclonal immune activation [31]. It is well established that NK cells have a crucial role in the initial defense against viral infections [32].

    • The role of tunable activation thresholds in the dynamics of autoimmunity

      2012, Journal of Theoretical Biology
      Citation Excerpt :

      There are many mechanisms by which host infection by a pathogen may contribute to autoimmunity, including triggering the innate immune system, molecular mimicry and bystander activation (see, e.g., Ercolini and Miller, 2008 for a recent review). Molecular mimicry is thought to be particularly important when viruses cause autoimmunity (Ercolini and Miller, 2008; Fujinami, 2001; Münz et al., 2009; von Herrath and Oldstone, 1996). An immune response elicited against a viral protein that mimics a self-antigen will not only eliminate the virus, but can also target normal host cells that display the cross-reactive self-antigen.

    • Experimental autoimmune encephalomyelitis as a testing paradigm for adjuvants and vaccines

      2011, Vaccine
      Citation Excerpt :

      Modulation of the disease course of EAE could be a useful animal model for exacerbations of disease that occur in MS patients in association with viral infections (reviewed in [28]). Immunization or vaccination of MS patients has not been found to be associated with exacerbations (reviewed in [9]). Administration of CNS proteins/peptides by means of a live viral infection has been shown to protect the animal against the later development of EAE [29,30].

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