Differential Effects of Glucocorticosteroids on the Functions of Helper and Suppressor T Lymphocytes

The effects of dexamethasone (Dex) on the functions of antigen-primed helper and suppressor T cells were studied in humoral immune responses in vitro. In doses equivalent to elevated physiologic concentrations, the suppressor T cell activity was abolished. In contrast, the helper T cell function was...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1981-05, Vol.78 (5), p.3155-3159
Main Authors: Bradley, Linda M., Mishell, Robert I.
Format: Article
Language:English
Subjects:
Animals
Antibody Formation - drug effects
Cell growth
Cultured cells
Dexamethasone - pharmacology
Erythrocytes
Immunization
Macrophage Migration-Inhibitory Factors - pharmacology
Macrophages
Mice
Mice, Inbred Strains
Physiological regulation
Spleen cells
Steroids
T lymphocytes
T-Lymphocytes - drug effects
T-Lymphocytes - immunology
T-Lymphocytes - radiation effects
T-Lymphocytes, Regulatory - drug effects
T-Lymphocytes, Regulatory - immunology
Transplantation immunology
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Summary:The effects of dexamethasone (Dex) on the functions of antigen-primed helper and suppressor T cells were studied in humoral immune responses in vitro. In doses equivalent to elevated physiologic concentrations, the suppressor T cell activity was abolished. In contrast, the helper T cell function was resistant to even pharmacologic concentrations of Dex. The apparent steroid resistance of the helper T cells was found to be mediated by the products of activated macrophages. While macrophage factors protected helper T cells from steroid inhibition, they did not prevent the effects of Dex on suppressor T cells. Because bacterial cell wall and membrane components are potent inducers of the factors that mediate steroid resistance of helper T cells, the combination of physiologically elevated levels of steroids and macrophage factors during acute infections may function to facilitate the expression of host immunity. However, the persistance of these conditions, as in chronic inflammation, may also contribute to the pathogenesis of autoimmunity by perturbing the balance of immune regulation by helper and suppressor T cells.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.78.5.3155