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Different T\u2010lymphocyte subsets are involved in the immune response against\n                    <jats:italic>M. tuberculosis<\/jats:italic>\n                    , but production of interferon\u2010gamma (IFN\u2010\n                    <jats:italic>\u03b3<\/jats:italic>\n                    ) by T cells seems to be fundamental for disease control. Th1\u2010type cytokine responses predominate in patients with mild or moderate forms of pulmonary TB, whereas the production of Th2\u2010type cytokines prevails in the severe disease. Since the immune response fails to definitely eradicate the pathogen, a chronic infection is established, and it is likely that a broad range of regulatory mechanisms operate in this situation. Cytokines released during the course of an immune response activate the hypothalamus\u2010pituitary\u2010adrenal axis leading to the production of glucocorticoids and dehydroepiandrosterone (DHEA), with known immunomodulatory effects. TB patients exhibit increased concentrations of interleukin\u20106 and cortisol in plasma, reduced DHEA and testosterone levels, together with remarkably increased growth hormone concentrations that were not accompanied by an expected raise in insulin\u2010like growth factor\u20101. Significant increases in estradiol, prolactin, and thyroid hormone concentrations were also detected in patients. Cortisol inhibits the mycobacterial antigen\u2010driven proliferation and IFN\u2010\n                    <jats:italic>\u03b3<\/jats:italic>\n                    production, whereas DHEA suppresses transforming growth factor beta production by lymphoid cells from TB patients with advanced disease. Furthermore, supernatants from cultures of\n                    <jats:italic>M. tuberculosis<\/jats:italic>\n                    \u2010stimulated mononuclear cells of TB patients inhibit DHEA secretion by a human adrenal cell line. This type of immuno\u2010endocrine interactions may affect the control of tissue damage and the development of protective immune responses, partly accounting for disease aggravation.\n                  <\/jats:p>","DOI":"10.1111\/j.1365-3083.2007.01962.x","type":"journal-article","created":{"date-parts":[[2007,6,20]],"date-time":"2007-06-20T12:47:51Z","timestamp":1182343671000},"page":"166-175","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":49,"title":["The Immuno\u2010endocrine Component in the Pathogenesis of Tuberculosis"],"prefix":"10.1111","volume":"66","author":[{"given":"O.","family":"Bottasso","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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