{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T21:48:35Z","timestamp":1757540915540},"reference-count":34,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,11,22]],"date-time":"2005-11-22T00:00:00Z","timestamp":1132617600000},"content-version":"vor","delay-in-days":6079,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1989,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Protective immunity against <jats:italic>Mycobacterium leprae<\/jats:italic> is dependent on <jats:italic>M. leprae<\/jats:italic>\u2010reactive T lymphocytes. <jats:italic>M. leprae<\/jats:italic>\u2010directed T cell reactivity is high in the localized tuberculoid form of leprosy but specifically absent in the disseminated lepromatous type of the disease.<\/jats:p><jats:p>Two important questions that are relevant for the understanding of the immune response in leprosy as well as for the design of rational immunoprophylaxis and \u2010therapy strategies are: (a) what are the antigens that trigger T cell responses in tuberculoid patients and thus protect these individuals from developing lepromatous leprosy and (b) is it possible to restore T cell responsiveness to <jats:italic>M. leprae<\/jats:italic> in lepromatous patients by rechallenging the immune system with selected antigens that will trigger help but not suppression? We have addressed these question by directly probing the peripheral T cell repertoire of 10 tuberculoid and 18 lepromatous patients with large numbers of different <jats:italic>M. leprae<\/jats:italic> and BCG antigenic components that had been separated on the basis of their relative molecular mass (M<jats:sub>r<\/jats:sub>) by sodium dodecyl sulfate\u2010polyacrylamide gel electrophoresis and electroblotted onto nitrocellulose. This technique allows the identification of T cell\u2010stimulating antigens independent of the expression of B cell epitopes by these antigens. So far T cell epitopes have only been mapped on <jats:italic>M. leprae<\/jats:italic> proteins that had previously been defined by antibodies. Our results show that: (a) tuberculoid patients' T cells responded preferentially to <jats:italic>M. leprae<\/jats:italic> and BCG antigens in the lower (<jats:italic>i.e.<\/jats:italic> &lt; 70 kDa) M<jats:sub>r<\/jats:sub> range with a peak in the 10\u201325 kDa range; (b) 6 out of 18 lepromatous patients that did not respond to whole <jats:italic>M. leprae<\/jats:italic> responded strongly to isolated <jats:italic>M. leprae<\/jats:italic> components; antigens in the lower M<jats:sub>r<\/jats:sub>. range were recognized by five out of these six patients and thus commonly seen by both tuberculoid and lepromatous patients' T cells; however, antigens in the higher M<jats:sub>r<\/jats:sub> range, in particular &gt; 150 kDa, were only recognized by lepromatous patients' T lymphocytes; (c) furthermore, the T and B cell repertoires in leprosy patients are skewed towards different antigenic fractions.<\/jats:p>","DOI":"10.1002\/eji.1830190421","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T10:48:44Z","timestamp":1172746124000},"page":"707-713","source":"Crossref","is-referenced-by-count":30,"title":["T cell responses to fractionated <i>Mycobacterium leprae<\/i> antigens in leprosy. The lepromatous nonresponder defect can be overcome <i>in vitro<\/i> by stimulation with fractionated <i>M. leprae<\/i> components"],"prefix":"10.1002","volume":"19","author":[{"given":"Tom H. M.","family":"Ottenhoff","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul J.","family":"Converse","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Negussie","family":"Gebre","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Assefa","family":"Wondimu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John P.","family":"Ehrenberg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rolf","family":"Kiessling","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,11,22]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/clinids\/5.4.765"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.1984.tb00493.x"},{"key":"e_1_2_1_4_2","first-page":"121","volume":"64","author":"Gill H. 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