Open AccessProtective effect of transforming growth factor beta 1 on experimental autoimmune diseases in mice.
Author(s) -
A P Kuruvilla,
Rutvi Shah,
G. M. Hochwald,
H. Denny Liggitt,
Michael A. Palladino,
G. J. Thorbecke
Publication year - 1991
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.88.7.2918
Subject(s) - rheumatoid arthritis , experimental autoimmune encephalomyelitis , immunology , medicine , transforming growth factor beta , autoimmune disease , multiple sclerosis , beta (programming language) , tumor necrosis factor alpha , transforming growth factor , arthritis , encephalomyelitis , tgf beta signaling pathway , autoimmunity , immune system , antibody , computer science , programming language
Interleukin 1 (IL-1) and tumor necrosis factor alpha are thought to contribute to the inflammatory response associated with autoimmune diseases. Transforming growth factor beta 1 (TGF-beta 1) counteracts many effects of these cytokines and has various immunosuppressive properties. In the present study, it is shown that microgram amounts of TGF-beta 1, injected daily for 1-2 weeks, protect against collagen-induced arthritis (CIA) and relapsing experimental allergic encephalomyelitis (REAE), the animal models for rheumatoid arthritis and multiple sclerosis, respectively. When administered during induction of the disease, TGF-beta 1 prevents CIA but only delays the onset of REAE by 2-3 days. However, when administered during a remission. TGF-beta 1 prevents the occurrence of relapses in REAE. The results suggest that TGF-beta 1 has powerful anti-inflammatory effects, mimicking in some respects the beneficial effects of immunosuppressive drugs in these experimental models of autoimmune disease, but without discernable adverse effects.