The hygiene hypothesis in autoimmunity: the role of pathogens and commensals.
Level 5 - mechanism / opinion, no new human data
Narrative review and mechanism-based reasoning without systematic methodology
PubMed 29034905 · doi:10.1038/nri.2017.111
What was done
This narrative review examines the hygiene hypothesis in the context of autoimmunity, synthesizing epidemiological observations, preclinical infection models (bacteria, viruses, and parasites), and mechanistic evidence on how pathogens and gut commensals interact with innate immune receptors such as Toll-like receptors (TLRs).
What was found
The abstract reports no numerical findings or statistical metrics. It describes an inverse epidemiological relationship between declining infectious disease incidence and rising autoimmune and allergic disease incidence. Preclinical models demonstrate that various infections can prevent autoimmune disease, and clinical observations show gut dysbiosis in autoimmune patients, driven mechanistically by pathogen- and commensal-mediated stimulation of immunoregulatory pathways via innate immune receptors.
Why it matters
The review outlines how innate immune signaling mediated by microbes may suppress autoimmune pathways, providing conceptual targets for understanding immune regulation.
Limits
The abstract contains no primary quantitative data or systematic review methodology. A causal link between human gut dysbiosis and the onset of autoimmune disease remains unestablished, and much of the mechanistic evidence relies on animal models.
Cited by
- supports Autoimmune and autoinflammatory diseases are significantly less prevalent in countries with higher early-life exposure to environmental infections compared to cleaner, industrialized nations.