Long-term treatment of chronic relapsing experimental allergic encephalomyelitis by transforming growth factor-beta 2.
It had been demonstrated previously that the administration of transforming growth factor-beta 1 (TGF-beta 1) reduced the clinical severity of experimental allergic encephalomyelitis (EAE). Treatment with the related immunosuppressive molecule, TGF-beta 2, resulted in similar inhibition of T cell activation and proliferation in vitro. Long-term treatment was effective in reducing clinical severity of EAE and the number of relapses in mice receiving either myelin basic protein- or peptide-91-103-specific T cell lines. When examined histologically, mice that had received TGF-beta 2 demonstrated significantly less inflammation and demyelination in the central nervous system. Examination of other organs demonstrated no pathology or deleterious side effects from long-term TGF-beta 2 therapy. These findings have relevance for the use of TGF-beta 2 as a therapeutic agent for the human demyelinating disease, multiple sclerosis.
Racke
M K
MK
Neuroimmunology Branch, NINDS, Bethesda, MD 20892.
Sriram
S
S
Carlino
J
J
Cannella
B
B
Raine
C S
CS
McFarlin
D E
DE
D000595:Amino Acid Sequence; D000818:Animals; D002908:Chronic Disease; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000517:prevention & control / Q000628:therapy*; D005260:Female; D008213:Lymphocyte Activation / Q000187:drug effects; D051379:Mice; D008815:Mice, Inbred Strains; D008969:Molecular Sequence Data; D004676:Myelin Basic Protein / Q000737:chemistry / Q000276:immunology*; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000627:therapeutic use*
D004676:Myelin Basic Protein; D016212:Transforming Growth Factor beta