Abstract：
:The interaction over time of genetic, epigenetic and environmental factors (i.e., autoimmune ecology) increases or decreases the liability an individual would have to develop an autoimmune disease (AD) depending on the misbalance between risk and protective effects. Pathogens have been the most common antecedent events studied, but multiple other environmental factors including xenobiotic chemicals, drugs, vaccines, and nutritional factors have been implicated into the development of ADs. Three main mechanisms have been offered to explain the development of autoimmunity: molecular mimicry, epitope spreading, and bystander activation. The latter is characterized by auto-reactive B and T cells that undergo activation in an antigen-independent manner, influencing the development and course of autoimmunity. Activation occurs due to a combination of an inflammatory milieu, co-signaling ligands, and interactions with neighboring cells. In this review, we will discuss the studies performed seeking to define the role of bystander activation in systemic and organ-specific ADs. In all cases, we are cognizant of individual differences between hosts and the variable latency time for clinical expression of disease, all of which have made our understanding of the etiology of loss of immune tolerance difficult and enigmatic.
journal_name
J Autoimmunjournal_title
Journal of autoimmunityauthors
Pacheco Y,Acosta-Ampudia Y,Monsalve DM,Chang C,Gershwin ME,Anaya JMdoi
10.1016/j.jaut.2019.06.012subject
Has Abstractpub_date
2019-09-01 00:00:00pages
102301eissn
0896-8411issn
1095-9157pii
S0896-8411(19)30314-2journal_volume
103pub_type
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pub_type： 杂志文章
doi：10.1016/0896-8411(89)90172-8
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pub_type： 社论,历史文章
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journal_title：Journal of autoimmunity
pub_type： 杂志文章,评审
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pub_type： 杂志文章
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journal_title：Journal of autoimmunity
pub_type： 杂志文章,评审
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更新日期：2020-02-01 00:00:00
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