Proceedings of the National Academy of Sciences · 1991 · 408 citations · 43 references
MedicineImmunologyPathologyAutoimmunityInflammationRheumatologyAutoimmune Disease PathogenesisAutoimmune DiseasesAutoimmune InflammationInflammatory ArthritisInflammatory SignalingRheumatoid ArthritisCollagen-induced ArthritisCytokine Signaling In AutoimmunityExperimental Autoimmune EncephalomyelitisImmunosuppressive FunctionTransforming Growth Factor Beta-mediated Immune SuppressionTransforming Growth Factor-beta Signaling
TGF‑β1 counteracts pro‑inflammatory cytokines IL‑1 and TNF‑α and possesses immunosuppressive properties. Microgram daily doses of TGF‑β1 for 1–2 weeks protect mice from collagen‑induced arthritis and relapsing experimental allergic encephalomyelitis, prevent CIA when given at induction, delay REAE onset by 2–3 days, and avert relapses, demonstrating potent anti‑inflammatory effects comparable to immunosuppressive drugs without discernible adverse effects. No benefit was observed when TGF‑β1 was administered during remission.
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.
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John H. Kehrl, Lalage M. Wakefield, Anita B. Roberts et al. · The Journal of Experimental Medicine · 1986 · 1.6K citations · Full text
Deactivation of macrophages by transforming growth factor-β
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