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Transforming growth factor-beta 1 in experimental autoimmune neuritis. Cellular localization and time course
R Kiefer1, K Funa, T Schweitzer
1Department of Neurology, University of Würzburg, Germany.
The American Journal of Pathology
|January 1, 1996
Summary
Transforming growth factor-beta 1 (TGF-beta 1) is upregulated during experimental autoimmune neuritis (EAN) recovery in rats. This immunosuppressive cytokine, primarily from macrophages, may mediate spontaneous peripheral nervous system healing.
Area of Science:
- Neuroimmunology
- Peripheral Nervous System Disorders
- Cytokine Signaling
Background:
- Experimental autoimmune neuritis (EAN) is a peripheral nervous system inflammatory disorder with unknown spontaneous resolution mechanisms.
- The role of endogenous immunosuppressive cytokines in EAN recovery is not well understood.
Purpose of the Study:
- To investigate the endogenous expression of transforming growth factor-beta 1 (TGF-beta 1) in the peripheral nervous system during EAN in Lewis rats.
- To identify the cellular sources of TGF-beta 1 during EAN and its potential role in spontaneous recovery.
Main Methods:
- Quantitative Northern blot analysis and in situ hybridization histochemistry to detect TGF-beta 1 mRNA.
- Immunocytochemistry to visualize TGF-beta 1 protein.
- Double labeling studies to identify TGF-beta 1 expressing cells.
Main Results:
- TGF-beta 1 mRNA and protein levels were significantly upregulated in the peripheral nervous system during EAN, peaking before clinical recovery.
- Macrophages and T cells were identified as major cellular sources of TGF-beta 1 mRNA.
- Constitutive expression of TGF-beta 1 was also observed in axons and Schwann cells.
Conclusions:
- Endogenous TGF-beta 1 elaboration in the peripheral nerve may mediate the spontaneous recovery from EAN.
- Macrophages may regulate their own cytotoxicity through TGF-beta 1 expression during EAN.