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Related Experiment Video

Updated: Aug 19, 2025

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

Published on: December 17, 2010

Autoimmune pre-disease.

Katja Bieber¹, Jennifer E Hundt¹, Xinhua Yu²

¹Lübeck Institute of Experimental Dermatology and Center for Research on Inflammation of the Skin, University of Lübeck, Germany.

Autoimmunity Reviews

|November 27, 2022

Summary

This summary is machine-generated.

Identifying biomarkers for autoimmune disease progression is crucial. This review explores the transition from harmless autoimmunity to clinical disease, highlighting current knowledge gaps and future research directions.

Keywords:

Autoimmunity Diet Drugs Environment Pathogenesis Pre-disease Shift work Smoking

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Published on: March 17, 2023

Area of Science:

Immunology
Autoimmunity
Disease Pathogenesis

Background:

Autoimmune diseases affect 5% of the global population, posing significant treatment challenges and economic burdens.
Disease development is a multi-year process involving autoantigen-specific lymphocytes and autoantibodies, but not all individuals with autoantibodies develop clinical symptoms.
Identifying and intervening in the transition from harmless autoimmunity to inflammatory conditions is a critical unmet need.

Purpose of the Study:

To review the current understanding of autoimmune disease progression from health to clinically manifest disease.
To identify knowledge gaps in defining and modulating the autoimmune predisease phase.
To outline future research perspectives for targeting autoimmune predisease.

Main Methods:

Review of published scientific literature on autoimmune disease development.
Analysis of factors influencing the transition from harmless to inflammatory autoimmune responses.
Synthesis of current status, missing knowledge, and future directions in autoimmune predisease research.

Main Results:

The switch to inflammatory autoantigen-specific T and B-cell responses is a key factor in disease manifestation.
Biomarkers predicting progression from autoantibody presence to clinical disease are lacking.
Environmental and genetic factors significantly influence disease progression.

Conclusions:

Defining and targeting the autoimmune predisease phase holds significant therapeutic potential.
Further research is needed to develop predictive biomarkers and therapeutic strategies for autoimmune predisease.
Understanding the transition from harmless autoimmunity to inflammatory disease is essential for effective intervention.