Protective effect of transforming growth factor beta 1 on experimental autoimmune diseases in mice. 1991

A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
Department of Pathology, Kaplan Cancer Center, New York University School of Medicine, NY 10016.

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.

UI MeSH Term Description Entries
D008811 Mice, Inbred DBA An inbred strain of mouse. Specific substrains are used in a variety of areas of BIOMEDICAL RESEARCH such as DBA/1J, which is used as a model for RHEUMATOID ARTHRITIS. Mice, DBA,Mouse, DBA,Mouse, Inbred DBA,DBA Mice,DBA Mice, Inbred,DBA Mouse,DBA Mouse, Inbred,Inbred DBA Mice,Inbred DBA Mouse
D008815 Mice, Inbred Strains Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation. Inbred Mouse Strains,Inbred Strain of Mice,Inbred Strain of Mouse,Inbred Strains of Mice,Mouse, Inbred Strain,Inbred Mouse Strain,Mouse Inbred Strain,Mouse Inbred Strains,Mouse Strain, Inbred,Mouse Strains, Inbred,Strain, Inbred Mouse,Strains, Inbred Mouse
D011994 Recombinant Proteins Proteins prepared by recombinant DNA technology. Biosynthetic Protein,Biosynthetic Proteins,DNA Recombinant Proteins,Recombinant Protein,Proteins, Biosynthetic,Proteins, Recombinant DNA,DNA Proteins, Recombinant,Protein, Biosynthetic,Protein, Recombinant,Proteins, DNA Recombinant,Proteins, Recombinant,Recombinant DNA Proteins,Recombinant Proteins, DNA
D012008 Recurrence The return of a sign, symptom, or disease after a remission. Recrudescence,Relapse,Recrudescences,Recurrences,Relapses
D003094 Collagen A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH). Avicon,Avitene,Collagen Felt,Collagen Fleece,Collagenfleece,Collastat,Dermodress,Microfibril Collagen Hemostat,Pangen,Zyderm,alpha-Collagen,Collagen Hemostat, Microfibril,alpha Collagen
D004681 Encephalomyelitis, Autoimmune, Experimental An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5) Autoimmune Encephalomyelitis, Experimental,Encephalomyelitis, Allergic,Encephalomyelitis, Experimental Autoimmune,Allergic Encephalomyelitis,Allergic Encephalomyelitis, Experimental,Autoimmune Experimental Encephalomyelitis,Experimental Allergic Encephalomyelitis,Experimental Autoimmune Encephalomyelitis,Encephalomyelitis, Autoimmune Experimental,Encephalomyelitis, Experimental Allergic,Experimental Allergic Encephalomyelitides,Experimental Encephalomyelitis, Autoimmune
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D001169 Arthritis, Experimental ARTHRITIS that is induced in experimental animals. Immunological methods and infectious agents can be used to develop experimental arthritis models. These methods include injections of stimulators of the immune response, such as an adjuvant (ADJUVANTS, IMMUNOLOGIC) or COLLAGEN. Adjuvant Arthritis,Arthritis, Adjuvant-Induced,Arthritis, Collagen-Induced,Arthritis, Adjuvant,Collagen Arthritis,Arthritides, Collagen,Arthritis, Collagen,Collagen Arthritides,Collagen-Induced Arthritides,Collagen-Induced Arthritis

Related Publications

A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
November 1997, Nippon Ganka Gakkai zasshi,
A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
June 1994, Cellular immunology,
A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
August 2000, Zeitschrift fur Gastroenterologie,
A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
March 1999, Infection and immunity,
A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
February 1996, Molecular pharmacology,
A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
February 2000, Journal of autoimmunity,
A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
January 1996, The American journal of pathology,
A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
February 1996, Blood,
A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
June 2014, Allergy,
A P Kuruvilla, and R Shah, and G M Hochwald, and H D Liggitt, and M A Palladino, and G J Thorbecke
February 2000, Journal of molecular and cellular cardiology,
Copied contents to your clipboard!