Prevention and treatment of chronic relapsing experimental allergic encephalomyelitis by transforming growth factor-beta 1
- PMID: 1707929
Prevention and treatment of chronic relapsing experimental allergic encephalomyelitis by transforming growth factor-beta 1
Abstract
Experimental allergic encephalomyelitis (EAE) is an autoimmune disease characterized by inflammation and demyelination in the central nervous system. The effect of the immunosuppressive molecule transforming growth factor-beta, (TGF-beta 1) on chronic relapsing EAE produced by the transfer of myelin basic protein-specific T cell lines was studied. TGF-beta 1 markedly inhibited the activation and proliferation of myelin-basic protein-specific lymph node cells in vitro. This reduced the capacity of these cells to transfer EAE. In addition, administration of TGF-beta 1 in vivo consistently resulted in an improved clinical course, even when given during ongoing disease. Immunopathologic study demonstrated a marked reduction in central nervous system damage and expression of cell-surface lymphocyte function-associated Ag-1 and class II MHC molecules in TGF-beta 1-treated mice. These findings have identified TGF-beta 1 as a possible therapeutic agent for the human demyelinating disease multiple sclerosis.
Similar articles
-
Successful treatment of experimental allergic encephalomyelitis with transforming growth factor-beta 1.J Immunol. 1991 Sep 15;147(6):1792-6. J Immunol. 1991. PMID: 1716279
-
Retinoid treatment of experimental allergic encephalomyelitis. IL-4 production correlates with improved disease course.J Immunol. 1995 Jan 1;154(1):450-8. J Immunol. 1995. PMID: 7527821
-
Studies on the mechanisms by which transforming growth factor-beta (TGF-beta) protects against allergic encephalomyelitis. Antagonism between TGF-beta and tumor necrosis factor.J Immunol. 1993 Jul 15;151(2):1116-27. J Immunol. 1993. PMID: 8335893
-
Experimental allergic encephalomyelitis. T cell trafficking to the central nervous system in a resistant Thy-1 congenic mouse strain.Lab Invest. 1994 Nov;71(5):671-9. Lab Invest. 1994. PMID: 7526038
-
Has myelin basic protein received a fair trial in the treatment of multiple sclerosis?Ann Neurol. 1979 Dec;6(6):461-8. doi: 10.1002/ana.410060602. Ann Neurol. 1979. PMID: 93873 Review.
Cited by
-
Inflammation in EAE: role of chemokine/cytokine expression by resident and infiltrating cells.Neurochem Res. 1996 Apr;21(4):511-25. doi: 10.1007/BF02527717. Neurochem Res. 1996. PMID: 8734446 Review.
-
TGFβ in T cell biology and tumor immunity: Angel or devil?Cytokine Growth Factor Rev. 2014 Aug;25(4):423-35. doi: 10.1016/j.cytogfr.2014.07.014. Epub 2014 Jul 29. Cytokine Growth Factor Rev. 2014. PMID: 25156420 Free PMC article. Review.
-
The involvement of T cell receptor peptide-specific regulatory CD4+ T cells in recovery from antigen-induced autoimmune disease.J Exp Med. 1993 Sep 1;178(3):909-16. doi: 10.1084/jem.178.3.909. J Exp Med. 1993. PMID: 7688792 Free PMC article.
-
Subsets of transgenic T cells that recognize CD1 induce or prevent murine lupus: role of cytokines.J Exp Med. 1998 Feb 16;187(4):525-36. doi: 10.1084/jem.187.4.525. J Exp Med. 1998. PMID: 9463403 Free PMC article.
-
Experimental immunotherapies for multiple sclerosis.Springer Semin Immunopathol. 1996;18(1):1-24. doi: 10.1007/BF00792605. Springer Semin Immunopathol. 1996. PMID: 8984675 Free PMC article. Review.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Other Literature Sources
Research Materials