Important note: Information in this article was accurate in 1993. The state of the art may have changed since the publication date.
TNF and TGF-beta: the opposite sides of the avenue?
Tumor Necrosis Factors: The Molecules and Their Emerging Role in Medicine. Beutler B, ed. New York, Raven Press, p. 131-44, 1991.. Unique Identifier : AIDSLINE ICDB/93688881 Flynn RM; Palladino MA; Dept. of Cell Biology, Genentech, Inc., South San Francisco, CA; 94080
Abstract:
Cytokines, by modulating the synthesis and activities of additional factors with both agonist and antagonist functions, play a key role in regulating a highly controlled immune response. Some of the interactive immunoregulatory properties of transforming growth factor-beta (TGF-beta) and tumor necrosis factor (TNF) are described, including the balance of TGF-beta and TNF production and activities as an important homeostatic mechanism, in vitro immunoregulatory effects, and in vivo effects of TGF-beta and TNF. Many of the effects of TNF and TGF-beta on the immune system can be indirect by influencing the production of other immunoregulatory molecules. TNF can enhance the production of cytokines such as interleukin (IL)-1, IL-6, IL-8, granulocyte-macrophage colony-stimulating factor, granulocyte colony-stimulating factor, interferon-gamma, and its own synthesis. The effects of TGF-beta on cytokine production have been somewhat controversial. TNF and TGF-beta also have direct effects on various immune cell populations. TGF-beta is a potent inhibitor of thymocyte proliferation induced by multiple cytokines, including IL-1, IL-2, IL-4, IL-6, IL-7 and TNF. Both TNF and TGF-beta are important regulators of cytotoxic T-lymphocyte generation. TGF-beta 1 and TNF have been reported to exhibit variable effects on B-cell functions as well. Monocytes/macrophages play a central role in many cellular reactions, particularly in inflammatory responses and wound repair processes. Critical to the regulation of their activity is their interaction with TNF and TGF-beta. In many cellular systems and disease states, the effects of TGF-beta, TNF, and other members of the cytokine network appear to be in a critical balance that can dampen or enhance immune responses as needed. HIV has been able to utilize these homeostatic mechanisms of the immune system to optimize its own survival. Recently, an ability of TGF-beta to mediate cardioprotection during reperfusion in vivo has been reported. Although TGF-beta and TNF are important mediators of certain immune reactions, they are by no means the only keys to regulating immune responses. Ultimately, through carefully designed clinical trials, these two factors may be used to their max potential to treat or prevent disease. (87 Refs)
Keywords: Animal Macrophages/IMMUNOLOGY T-Lymphocytes/IMMUNOLOGY Transforming Growth Factor beta/*PHYSIOLOGY Tumor Necrosis Factor/*PHYSIOLOGY MONOGRAPH 930330
M9331105
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Important note: Information in this article was accurate in 1993. The state of the art may have changed since the publication date.
