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Novel Microbial Compounds as a Boon in Health Management
Published in Jyoti Ranjan Rout, Rout George Kerry, Abinash Dutta, Biotechnological Advances for Microbiology, Molecular Biology, and Nanotechnology, 2022
Shubha Rani Sharma, Rajani Sharma, Debasish Kar
by therapy due to radiation to avoid the rejection of the graft and also to control autoimmune diseases. There has been the discovery of numerous microbial compounds that are capable of immunosuppression. The most important immunosuppressants evolved in the form of Cyclosporin A. These immunosuppressants were produced by a mold Tolypocladium nivenum which was supposed to be a narrow spectrum antifungal by the process of aerobic fermentation (Isaac et al., 1990). Cyclosporins which were approved to be used as immunosuppressive drugs during transplants way back in 1983 are a family of microbial products. The mechanism of action of cyclosporin is seen to be its binding to immunophilin of T lymphocytes which is a cytosolic protein cyclophilin. This aids in the inactivation of transcription of interleukin-2, as well as inhibition of lymphokine production and, thus reduced the function of effector T cells.
Drug-Induced Autoimmunity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Robert L. Rubin, Anke Kretz-Rommel
Cyclosporine A is used therapeutically to suppress transplantation rejection, autoimmune disease and GVHD but is paradoxically related to development of certain types of autoimmunity. Most of these observations are in experimental animals, but it has been reported that withdrawal of cyclosporine after autologous bone marrow transplantation can result in an syndrome resembling GVHD.20,21 Treatment of neonatal mice with cyclosporine provokes organ-specific autommune disease,22 and certain strains of rat and mouse subjected to lethal irradiation followed by bone marrow reconstituition and treatment with cycolsporine for three or more weeks develop GVHD after withdrawal of cyclosporine.23
Pulmonary infection induced by drugs
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Marc B Feinstein, Dorothy A White
Ciclosporin, developed during the 1980s, and tacrolimus (formerly FK506), developed during the 1990s, exert their effects predominantly via helper T-lymphocytes by suppressing the transcription of IL-2 and a number of other inflammatory cytokines. These drugs have greatly improved the survival of solid-organ transplant recipients, and have also been effective against GVHD in allogeneic bone marrow or peripheral blood stem-cell transplant recipients as well as a number of rheumatologic and inflammatory conditions listed in Box 19.2.
Overview of biological mechanisms of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Nicholas Birkett, Mustafa Al-Zoughool, Michael Bird, Robert A. Baan, Jan Zielinski, Daniel Krewski
Ciclosporin enhances the synthesis of transforming growth factor β (TGF-β) and consequent activation of its dependent transcriptional activators. Studies in cultured human pulmonary adenocarcinoma cells treated with ciclosporin exhibited evidence of a metaplastic phenotype. It is not clear if this effect contributes to the carcinogenicity of ciclosporin.