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Th1 and Th2 lymphocytes in autoimmune disease
Isabel J Crane1, John V Forrester
1Department of Ophthalmology, University of Aberdeen Institute of Medical Sciences, Foresterhill, Aberdeen, AB25 2ZD, UK. i.j.crane@abdn.ac.uk
Critical Reviews in Immunology
|June 15, 2005
Summary
The Th1/Th2 paradigm helps understand autoimmune diseases like multiple sclerosis. New insights into T-cell regulation clarify exceptions and integrate the Th1/Th2 concept into complex autoimmune disease development.
Area of Science:
- Immunology
- Autoimmune Diseases
Background:
- The Th1/Th2 paradigm is a framework for understanding T-cell responses in autoimmune diseases.
- Evidence suggests diseases like multiple sclerosis and type 1 diabetes are Th1-mediated.
- However, numerous exceptions challenge the direct application of this paradigm.
Purpose of the Study:
- To re-evaluate the applicability of the Th1/Th2 paradigm in Th1-mediated autoimmune diseases.
- To address discrepancies and exceptions within the Th1/Th2 model.
- To integrate recent findings on T-cell regulation into the understanding of autoimmune disease pathogenesis.
Main Methods:
- Review of existing literature on Th1/Th2 responses in autoimmune diseases.
- Analysis of contradictory findings regarding Th1 cytokine (IFN-gamma) actions.
- Examination of the role of Th2 lymphocytes in disease pathogenesis.
- Inclusion of recent data on innate and adaptive immune regulation of T-cells.
Main Results:
- While some autoimmune diseases align with the Th1/Th2 model, many exceptions exist.
- The pleiotropic effects of IFN-gamma and the pathogenic potential of Th2 cells contribute to these exceptions.
- New understanding of T-cell regulation, including innate immune influences, helps explain discrepancies.
Conclusions:
- The Th1/Th2 paradigm requires nuanced application in Th1-mediated autoimmune diseases.
- Exceptions highlight the complexity of immune responses in autoimmunity.
- The Th1/Th2 concept remains integral but must be considered within a broader regulatory network involving innate immunity and other T-cell subsets.