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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

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Mechanisms of Environment-Induced Autoimmunity.

K Michael Pollard¹, David M Cauvi², Jessica M Mayeux¹

¹Department of Molecular Medicine, The Scripps Research Institute, La Jolla, California 92037, USA;

Annual Review of Pharmacology and Toxicology

|August 29, 2020

Summary

Environmental exposures, particularly particulate matter in the lungs, can trigger preclinical autoimmunity. Understanding these triggers is key to distinguishing early stages from clinical autoimmune diseases.

Keywords:

adaptive animal model autoimmunity environment inflammation innate xenobiotic

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Area of Science:

Environmental Medicine
Immunology
Pathology

Background:

Environmental exposures are implicated as triggers for preclinical autoimmunity, but few are definitively linked to autoimmune diseases.
The lungs are a common site for chronic environmental exposure, leading to cellular toxicity, inflammation, and fibrosis, especially with particulate matter.
Particulate exposure impairs clearance, prolongs inflammation, and contributes to the development of autoimmune responses.

Purpose of the Study:

To explore the link between environmental exposures and the development of autoimmune diseases.
To understand the mechanisms by which environmental factors initiate and exacerbate autoimmune processes.
To identify factors distinguishing preclinical autoimmunity from clinical autoimmune disease.

Main Methods:

Review of existing literature on environmental exposures and autoimmunity.
Analysis of pathological processes in the lung following exposure.
Examination of molecular and cellular events, including posttranslational modification of self-antigens and tertiary lymphoid structure formation.

Main Results:

Chronic lung exposure to environmental factors, especially particulate matter, promotes inflammation and tissue damage.
Posttranslational modification of self-antigens and B cell-rich tertiary lymphoid structures are associated with autoantibody generation.
Gene-environment interactions can lead to autoantibody responses with diagnostic specificity.

Conclusions:

Environmental exposures, particularly in the lungs, play a significant role in initiating autoimmune responses.
Understanding the transition from preclinical to clinical autoimmune disease is crucial for assessing environmental impact.
Further research into molecular and cellular mechanisms can clarify the role of environmental exposures in human autoimmune diseases.