title: Glucocorticoids and the immune function in the human immunodeficiency virus infection: a study in hypercortisolemic and cortisol-resistant patients.
abstract: Immunological studies in human immunodeficiency virus (HIV)-positive patients suggest that the disease progression is accompanied by a defective production of type 1 cytokines (interleukin-2 (IL-2) and IL-12], an increased production of type 2 cytokines (IL-4, IL-6, and IL-10), and an increased production of IgE. HIV infection is also associated with activation of the hypothalamo-pituitary-adrenal axis function and increased plasma and urinary cortisol concentrations. As cortisol is involved in the physiological regulation of cytokines, a study was conducted to examine cytokine patterns in two groups of hypercortisolemic patients, one with normal sensitivity to glucocorticoids and the other with glucocorticoid resistance. Ten HIV-infected patients with normal receptor affinity to glucocorticoids (AIDS-C), 10 HIV-infected patients with low receptor affinity to glucocorticoids (AIDS-GR), and 20 healthy subjects were studied. Receptor characteristics of peripheral blood mononuclear cells were evaluated by [3H]dexamethasone binding. Serum cortisol and urinary free cortisol were measured by RIA. Serum ACTH and IgE were measured by immunoradiometric assay, and IL-2, IL-4, and IL-10 cytokines and interferon-gamma were measured by enzyme-linked immunosorbent assay. AIDS-C patients showed low IL-2 and high IL-4, IL-10, and IgE concentratios; conversely, AIDS-GR patients showed high IL-2 and low IL-4 and IgE concentrations. Thus, in HIV infection, elevated cortisol levels suppress cell-mediated immunity and stimulate humoral immunity, whereas this response is not detected in cortisol-resistant patients. These findings indicate that cortisol and its receptors are critically involved in the regulation of immune function in HIV infection.
authors.affiliation: Department of Endocrinology, L. Sacco University Hospital, Milan, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Norbiato
authors.forename: M
authors.initials: M
authors.lastname: Bevilacqua
authors.forename: T
authors.initials: T
authors.lastname: Vago
authors.forename: A
authors.initials: A
authors.lastname: Taddei
authors.lastname: Clerici
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D016207:Cytokines / Q000097:blood; D003907:Dexamethasone / Q000378:metabolism; D004351:Drug Resistance; D005260:Female; D005938:Glucocorticoids / Q000378:metabolism / Q000627:therapeutic use*; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy* / Q000276:immunology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000627:therapeutic use* / Q000652:urine; D007107:Immune System / Q000187:drug effects* / Q000503:physiopathology*; D008297:Male; D009000:Monocytes / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D012016:Reference Values
chemical_list: D016207:Cytokines; D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone