Abstract
Here we show that stress exerts a differential effect on T-cell-dependent antibody production. IgG production is augmented after acute stress and impaired in a chronic situation. We found catecholamines and corticosterone levels were increased in acute situations although they were not modified after prolonged stress conditions. However, lymphocyte sensitivity to corticosterone and catecholamines was altered under stress conditions. These results point out the role of the adrenal's hormones as mediators of the differential effects of stress on the immune response providing the basis for a functional significance of stress hormone receptors on lymphocytes.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Acute Disease
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Animals
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Blood Group Antigens / administration & dosage
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Blood Group Antigens / immunology
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Catecholamines / biosynthesis
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Catecholamines / pharmacology
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Catecholamines / physiology*
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Cells, Cultured
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Chronic Disease
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Corticosterone / biosynthesis
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Corticosterone / pharmacology
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Corticosterone / physiology*
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Down-Regulation / immunology*
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Down-Regulation / physiology
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Female
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Immunoglobulin G / biosynthesis*
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Immunoglobulin G / physiology
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Lymphocyte Activation / physiology
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Mice
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Mice, Inbred BALB C
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Restraint, Physical
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Sheep
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Stress, Physiological / immunology*
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Stress, Physiological / metabolism*
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T-Lymphocyte Subsets / immunology*
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T-Lymphocyte Subsets / physiology
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Thymus Gland / immunology
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Up-Regulation / immunology*
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Up-Regulation / physiology
Substances
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Blood Group Antigens
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Catecholamines
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Immunoglobulin G
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Corticosterone