{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T17:44:29Z","timestamp":1761155069430},"reference-count":30,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1988,2,1]],"date-time":"1988-02-01T00:00:00Z","timestamp":570672000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Immunol Cell Biol"],"published-print":{"date-parts":[[1988,2]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Genetic susceptibility to infection with <jats:italic>M. leprae<\/jats:italic> was studied in 10 multiple case families of Australian Aborigines. Of the 87 members available for study, 24 had proven stable clinical leprosy which had been or was still being treated with diamino diphenyl sulphone. Evidence of contact with <jats:italic>M. leprae<\/jats:italic> in the remaining 63 members as assessed by ELISA to <jats:italic>M. leprae<\/jats:italic> sonicate and phenolic glycolipid (PGL) or by indirect immunofluorescence antibody assay was found in 78%, 64% and 71%, respectively. By contrast, <jats:italic>in vitro<\/jats:italic> assays of T cell function (LMAT and LTT) were less reliable indicators of exposure.<\/jats:p><jats:p>Evidence was sought for possible linkages between human leucocyte antigen (HLA) or non\u2010HLA genes and four marker phenotypes including clinical leprosy, clinical subtype of leprosy and lymphocyte transformation or leucocyte migration inhibition factor (LIF) production in response to <jats:italic>M. leprae<\/jats:italic> antigen. No associations were found with any particular HLA or non\u2010HLA gene. On the other hand, sequential analysis of the data from the 10 families was strongly suggestive of a linkage between HLA haplotype and non\u2010responsiveness to <jats:italic>M. leprae<\/jats:italic> as manifest by lack of LIF production but not lymphocyte transformation.<\/jats:p><jats:p>The model which best fits the data is for a gene on chromosome 6 in close linkage with the HLA haplotype, with two alleles, autosomal recessive inheritance and penetrance of 90%. On this basis, it can be suggested that disease type (lepromatous leprosy) rather than disease susceptibility may be controlled by genes within or closely linked to the major histocompatibility gene complex.<\/jats:p>","DOI":"10.1038\/icb.1988.2","type":"journal-article","created":{"date-parts":[[2007,7,20]],"date-time":"2007-07-20T07:56:56Z","timestamp":1184918216000},"page":"9-21","source":"Crossref","is-referenced-by-count":7,"title":["Leprosy and immunity: genetics and immune function in multiple case families"],"prefix":"10.1111","volume":"66","author":[{"given":"WD","family":"Rawlinson","sequence":"first","affiliation":[{"name":"Clinical Immunology Research Centre and Centenary Institute of Cancer Research and Cell Biology, University of Sydney N.S.W. 2006 Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Basten","sequence":"additional","affiliation":[{"name":"Clinical Immunology Research Centre and Centenary Institute of Cancer Research and Cell Biology, University of Sydney N.S.W. 2006 Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"WJ","family":"Britton","sequence":"additional","affiliation":[{"name":"Clinical Immunology Research Centre and Centenary Institute of Cancer Research and Cell Biology, University of Sydney N.S.W. 2006 Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"SW","family":"Serjeantson","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, John Curtin School of Medical Research, Australian National University Canberra City 2601 Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1988,2]]},"reference":[{"key":"e_1_2_1_2_1","first-page":"44","volume-title":"Leprosy","author":"Bryceson A","year":"1979"},{"key":"e_1_2_1_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00390238"},{"key":"e_1_2_1_4_1","first-page":"24","article-title":"HLA and susceptibility to leprosy","volume":"70","author":"Serjeantson S","year":"1982","journal-title":"Immunol. Rev."},{"key":"e_1_2_1_5_1","unstructured":"IMMLEP Report of the Sixth Meeting of the Scientific Working Group on the Immunology of Leprosy Geneva 7\u20139 June 1982."},{"key":"e_1_2_1_6_1","volume-title":"The Ninth International Histocompatibility Workshop","author":"Vries RRP","year":"1984"},{"key":"e_1_2_1_7_1","first-page":"211","article-title":"Immunological aspects of leprosy: Present status","volume":"25","author":"Godal T","year":"1978","journal-title":"Prog. Allergy"},{"key":"e_1_2_1_8_1","first-page":"95","article-title":"HLA class\u2010II immune response genes and products in leprosy","volume":"36","author":"Vries RRP","year":"1985","journal-title":"Prog. 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