The hygiene hypothesis in autoimmunity: the role of pathogens and commensals

J. -F. Bach

The hygiene hypothesis in autoimmunity: the role of pathogens and commensals

@article{Bach2018TheHH,
  title={The hygiene hypothesis in autoimmunity: the role of pathogens and commensals},
  author={J. -F. Bach},
  journal={Nature Reviews Immunology},
  year={2018},
  volume={18},
  pages={105-120}
}

J. -F. Bach
Published 2018 in Nature Reviews Immunology
DOI:10.1038/nri.2017.111

The incidence of autoimmune diseases has been steadily rising. Concomitantly, the incidence of most infectious diseases has declined. This observation gave rise to the hygiene hypothesis, which postulates that a reduction in the frequency of infections contributes directly to the increase in the frequency of autoimmune and allergic diseases. This hypothesis is supported by robust epidemiological data, but the underlying mechanisms are unclear. Pathogens are known to be important, as autoimmune… CONTINUE READING

View on Nature

Highly Cited

This paper has 25 citations. REVIEW CITATIONS

From This Paper

Figures, tables, and topics from this paper.

Figures & Tables

Citations

Publications citing this paper.

Sort by:

Concurrent cross-reactivity of microbiota-derived epitopes to both self and pathogens may underlie the "Hygiene hypothesis".

David Usharauli, Tirumalai Kamala

Scandinavian journal of immunology • 2018

View 3 Excerpts

Highly Influenced

The diabetes pandemic and associated infections: suggestions for clinical microbiology

Antonio Toniolo, Gianluca Cassani, +4 authors Ele Ferrannini

Reviews in medical microbiology : a journal of the Pathological Society of Great Britain and Ireland • 2019

View 1 Excerpt

Clindamycin Administration Increases the Incidence of Collagen-Induced Arthritis in Mice Through the Prolonged Impact of Gut Immunity

Shukai Yang, Huijuan Chen, +5 authors Jiecong Sun

Inflammation • 2018

View 1 Excerpt

Could Sodium Chloride be an Environmental Trigger for Immune-Mediated Diseases? An Overview of the Experimental and Clinical Evidence

Eric A Toussirot, Matthieu Béreau, Charline Vauchy, Philippe Saas

Front. Physiol. • 2018

View 1 Excerpt

References

Publications referenced by this paper.

Showing 1-10 of 196 references

Sort by:

Gut microbiota of Type 1 diabetes patients with good glycaemic control and high physical fitness is similar to people without diabetes: an observational study.

Christopher J Stewart, Andrea Nelson, +5 authors Daniel J. West

Diabetic medicine : a journal of the British Diabetic Association • 2017

Use of antibiotics in childhood and risk of Type 1 diabetes: a population-based casecontrol study

D Knights

Nat. Microbiol • 2017

Antibiotic-mediated gut microbiome perturbation accelerates development of type 1 diabetes in mice

Alexandra E Livanos, Thomas U. Greiner, +19 authors Martin J. Blaser

Nature Microbiology • 2016

Association between intestinal permeability and faecal microbiota composition in Italian children with beta cell autoimmunity at risk for type 1 diabetes.

Claudio Maffeis, Alessia Martina, +5 authors Giovanna E. Felis

Diabetes/metabolism research and reviews • 2016

Association of Early Exposure of Probiotics and Islet Autoimmunity in the TEDDY Study.

Ulla Uusitalo, Xiang Liu, +14 authors Suvi Mirjami Virtanen

JAMA pediatrics • 2016

Broad-Spectrum Antibiotic Treatment and Subsequent Childhood Type 1 Diabetes: A Nationwide Danish Cohort Study

Tine D Clausen, Thomas Bergholt, +5 authors Ellen Christine Leth Løkkegaard

PloS one • 2016

Endotoxin Tolerance Inhibits Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4 but Increases Expression and Activity of Protein Phosphatases.

Yanbao Xiong, Michael B Murphy, +5 authors Andrei E Medvedev

Journal of innate immunity • 2016

The hygiene hypothesis in autoimmunity: the role of pathogens and commensals

From This Paper

Figures, tables, and topics from this paper.

Figures & Tables

Explore Further: Topics Discussed in This Paper

Citations

Publications citing this paper.

Concurrent cross-reactivity of microbiota-derived epitopes to both self and pathogens may underlie the "Hygiene hypothesis".

The diabetes pandemic and associated infections: suggestions for clinical microbiology

Clindamycin Administration Increases the Incidence of Collagen-Induced Arthritis in Mice Through the Prolonged Impact of Gut Immunity

Could Sodium Chloride be an Environmental Trigger for Immune-Mediated Diseases? An Overview of the Experimental and Clinical Evidence

Dietary non-fermentable fiber prevents autoimmune neurological disease by changing gut metabolic and immune status

Enhanced TLR2 responses in multiple sclerosis

Genomic variation and strain-specific functional adaptation in the human gut microbiome during early life

Graves’ orbitopathy occurs sex-independently in an autoimmune hyperthyroid mouse model

Living inside the box: environmental effects on mouse models of human disease

Mast Cells Respond to Candida albicans Infections and Modulate Macrophages Phagocytosis of the Fungus

References

Publications referenced by this paper.

Gut microbiota of Type 1 diabetes patients with good glycaemic control and high physical fitness is similar to people without diabetes: an observational study.

Inflammasome activation in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE).

Mesenchymal stromal cells and autoimmunity.

Myeloid suppressor cells in cancer and autoimmunity.

Use of antibiotics in childhood and risk of Type 1 diabetes: a population-based casecontrol study

Antibiotic-mediated gut microbiome perturbation accelerates development of type 1 diabetes in mice

Association between intestinal permeability and faecal microbiota composition in Italian children with beta cell autoimmunity at risk for type 1 diabetes.

Association of Early Exposure of Probiotics and Islet Autoimmunity in the TEDDY Study.

Broad-Spectrum Antibiotic Treatment and Subsequent Childhood Type 1 Diabetes: A Nationwide Danish Cohort Study

Endotoxin Tolerance Inhibits Lyn and c-Src Phosphorylation and Association with Toll-Like Receptor 4 but Increases Expression and Activity of Protein Phosphatases.