Sequential expression of transforming growth factor-beta1 by T-cells, macrophages, and microglia in rat spinal cord during autoimmune inflammation - PubMed (original) (raw)
Sequential expression of transforming growth factor-beta1 by T-cells, macrophages, and microglia in rat spinal cord during autoimmune inflammation
R Kiefer et al. J Neuropathol Exp Neurol. 1998 May.
Abstract
Transforming growth factor-beta1 (TGF-beta1) is crucially involved in regulating inflammatory events during experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. Despite accumulating evidence for local expression of TGF-beta1 in the inflamed nervous system, uncertainty remains regarding its cellular source. We have investigated the temporospatial distribution of TGF-beta1 gene expression in rat spinal cord during EAE. In actively induced EAE, in situ hybridization revealed strong expression of TGF-beta1 in meningeal and perivascular mononuclear infiltrates at onset of the disease, continued expression in perivascular infiltrates and scattered mononuclear cells at maximal disease severity, and expression in scattered parenchymal cells during recovery. Double labeling studies revealed subpopulations of infiltrating T-cells to be the major source of TGF-beta1 early in the disease, followed by macrophages at peak severity and microglial cells during the recovery phase of EAE. Astrocytes and neurons did not express TGF-beta1. Quantification of mRNA by Northern blot analysis revealed that cellular expression of TGF-beta1 by T-cells, macrophages, and microglia sums up to a long-lasting elevation of TGF-beta1 mRNA extending well into the recovery phase. Our data indicate cellular diversity and suggest functional diversity of TGF-beta1 gene expression during EAE. While TGF-beta1 expressed early in the disease by T-cells may contribute to inflammatory lesion development, microglial cells may potentially contribute to recovery by expressing immunosuppressive TGF-beta1 during remission.
Similar articles
- Differential expression of fibroblast growth factor-2 and receptor by glial cells in experimental autoimmune encephalomyelitis (EAE).
Gehrmann J, Lannes-Vieira J, Wekerle H. Gehrmann J, et al. Glia. 1996 Feb;16(2):93-100. doi: 10.1002/(SICI)1098-1136(199602)16:2<93::AID-GLIA1>3.0.CO;2-B. Glia. 1996. PMID: 8929896 Retracted. - Transforming growth factor beta expression in reactive spinal cord microglia and meningeal inflammatory cells during experimental allergic neuritis.
Kiefer R, Gold R, Gehrmann J, Lindholm D, Wekerle H, Kreutzberg GW. Kiefer R, et al. J Neurosci Res. 1993 Nov 1;36(4):391-8. doi: 10.1002/jnr.490360405. J Neurosci Res. 1993. PMID: 7505838 - Adoptive transfer of genetically modified macrophages elucidated TGF-beta-mediated 'self-defence' of the glomerulus against local action of macrophages.
Kitamura M. Kitamura M. Nephrol Dial Transplant. 1999;14 Suppl 1:35-8. doi: 10.1093/ndt/14.suppl_1.35. Nephrol Dial Transplant. 1999. PMID: 10048446 Review. - Transforming growth factor-beta 1: a lesion-associated cytokine of the nervous system.
Kiefer R, Streit WJ, Toyka KV, Kreutzberg GW, Hartung HP. Kiefer R, et al. Int J Dev Neurosci. 1995 Jun-Jul;13(3-4):331-9. doi: 10.1016/0736-5748(94)00074-d. Int J Dev Neurosci. 1995. PMID: 7572285 Review.
Cited by
- Involvement of tissue plasminogen activator in onset and effector phases of experimental allergic encephalomyelitis.
Lu W, Bhasin M, Tsirka SE. Lu W, et al. J Neurosci. 2002 Dec 15;22(24):10781-9. doi: 10.1523/JNEUROSCI.22-24-10781.2002. J Neurosci. 2002. PMID: 12486171 Free PMC article. - Fibrotic Scar in CNS Injuries: From the Cellular Origins of Fibroblasts to the Molecular Processes of Fibrotic Scar Formation.
Ayazi M, Zivkovic S, Hammel G, Stefanovic B, Ren Y. Ayazi M, et al. Cells. 2022 Aug 2;11(15):2371. doi: 10.3390/cells11152371. Cells. 2022. PMID: 35954214 Free PMC article. Review. - Early Blockade of TLRs MyD88-Dependent Pathway May Reduce Secondary Spinal Cord Injury in the Rats.
Yao AH, Jia LY, Zhang YK, Ma QR, Cheng P, Liu L, Ju G, Kuang F. Yao AH, et al. Evid Based Complement Alternat Med. 2012;2012:591298. doi: 10.1155/2012/591298. Epub 2012 May 22. Evid Based Complement Alternat Med. 2012. PMID: 22675384 Free PMC article. - Mechanism of experimental autoimmune encephalomyelitis in Lewis rats: recent insights from macrophages.
Shin T, Ahn M, Matsumoto Y. Shin T, et al. Anat Cell Biol. 2012 Sep;45(3):141-8. doi: 10.5115/acb.2012.45.3.141. Epub 2012 Sep 30. Anat Cell Biol. 2012. PMID: 23094201 Free PMC article. - Role of microglia in neurotrauma.
Loane DJ, Byrnes KR. Loane DJ, et al. Neurotherapeutics. 2010 Oct;7(4):366-77. doi: 10.1016/j.nurt.2010.07.002. Neurotherapeutics. 2010. PMID: 20880501 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources