Abstract
Host reaction to the changes in homeostatic balance induced by infection or neoplasia is characterized by a complex, but carefully orchestrated series of events called inflammation. Cells involved in this process communicate with their environment, and themselves, through multi-directional networks of inflammatory signals (cytokines) that induce, amplify, or suppress particular responses. Analysis of the cells that are involved in inflammation repeatedly points to a single cell in control: the macrophage. These cells serve not only as the initiators of antigen-specific immunity through antigen processing and presentation, but also as effector cells for elimination of the offending pathogen once Immunity has been established. Of particular interest in recent years has been the signals and sequence of events that regulate the onset of nonspecific cytotoxic effector reactions of macrophages. This interest initiated from the original studies of Mackaness, who observed that mice infected with one bacterium were able to survive normally lethal infections with completely unrelated bacteria. After years of experimental analysis, it became clear that the cellular basis for this nonspecific resistance had two obligate components: T lymphocytes and macrophages. Immune T cells respond to antigen in context of histocompatability antigens on the macrophage, and release hormone-like cytokines (lymphokines, LK), that regulate macrophage function. A subset of these LK, in turn, activates macrophages to become nonspecific killer cells. These activated cells can now eliminate not only the inciting infectious agent that induced the immune response, but also a wide variety of completely unrelated viral, bacterial, fungal, parasitic, and neoplastic targets. The activation of macrophages for nonspecific cytotoxic effector functions occurs early in the evolution of an immune response, and constitutes the host’s first opportunity for containment of the invading microorganism.
Keywords
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Hoover, D.L. and C.A. Nacy. 1984. Macrophage activation to kill Leishmania tropica: defective intracellular destruction of amastigotes by macrophages elicited by sterile inflammatory agents. J. Immunol. 132: 1487–1493.
Meltzer, M.S. and C.A. Nacy. 1985. Macrophage cytotoxlcity against tumor cell and microbial targets: genetic control of the activation network. Prog. Leuk. Biol. 3: 595–604.
Meltzer, M.S., D.L. Hoover, M.J. Gilbreath, R.D. Schreiber, and C.A. Nacy. 1986. Experimental variables for induction of activated cytotoxic macrophages. Ann. Inst. Pasteur/Immunol. 137C: 206–211.
Nacy, C.A., M.S. Meltzer, E.J. Leonard, and D.J. Wyler. 1981. Intracellular replication and lymphokine-Induced destruction of Leishmania tropica in C3H/HeN mouse macrophages. J. Immunol. 127: 2381–2386.
Nacy, C.A. and M.S. Meltzer. 1979. Macrophages in resistance to rickettsia) Infection: macrophage activation in vitro for killing of Rickettsia tsutsugamushi. J. Immunol. 123: 2544–2549.
Nacy, C.A., E.J. Leonard and M.S. Meltzer. 1981. Macrophages in resistance to rickettsia) Infections: characterization of lymphokines that induce rickettsiacidal activity in macrophages. J. Immunol. 126: 204–207.
Nacy, C.A., C.N. Oster, S.L. James, and M.S. Meltzer. 1984. Activation of macrophages for destruction of Intracellular and extraceilular parasites. Cont. Topics immunobiol. 14: 147–170.
Nacy, C.A. 1984. Macrophage activation to kill Leishmania tropica: Identification of a soluble T cell factor that suppresses lymphokine-induced Intracellular killing of amastigotes. J. Immunol. 133: 448453
Nacy, C.A., A.H. Fortier, M.S. Meltzer, N.A. Buchmeier, and R.D. Schreiber. 1985. Macrophage activation to kill Leishmania tropica: macrophages can be activated to kill amastigotes by both interferon gamma and non-interferon lymphokines. J. Immunol. 135: 3505–3511.
Nacy, C.A., C.E. Davis, B.A. Mock, M.J. Gilbreath, and M.S. Meltzer. 1986. Regulation of macrophage antimicrobial activities by lymphocyte products. Clin. Immunol. Newsletter 7: 65–69.
Oster, C.N. and C.A. Nacy. 1984. Macrophage activation to kill Leishmania tropica: kinetics of macrophage response to lymphokines that Induce microbicidal activities against Leishmania tropica amastigotes. J. Immunol. 132: 1494–1500.
Pappas, M.G., C.N. Oster, and C.A. Nacy. 1982. Intracellular destruction of Leishmania tropica by macrophages activated in vivo with Mycobacterium bovis strain BCG. Adv. Exp. Med. Biol. 162: 425–431.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1988 Springer Science+Business Media New York
About this chapter
Cite this chapter
Nacy, C.A., Belosevic, M., Crawford, R.M., Healy, A.T., Schreiber, R.D., Meltzer, M.S. (1988). Lymphokine Regulation of Macrophage Effector Activities. In: Eisenstein, T.K., Bullock, W.E., Hanna, N. (eds) Host Defenses and Immunomodulation to Intracellular Pathogens. Advances in Experimental Medicine and Biology, vol 239. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-5421-6_1
Download citation
DOI: https://doi.org/10.1007/978-1-4757-5421-6_1
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4757-5423-0
Online ISBN: 978-1-4757-5421-6
eBook Packages: Springer Book Archive