{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T14:50:40Z","timestamp":1792594240567,"version":"4.5.0"},"reference-count":90,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2016,4,22]],"date-time":"2016-04-22T00:00:00Z","timestamp":1461283200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Leprosy is a disease caused by Mycobacterium leprae that presents on a spectrum of both clinical manifestations and T cell response. On one end of this spectrum, tuberculoid leprosy is a well-controlled disease, characterized by a cell-mediated immunity and immunosurveillance. On the opposite end of the spectrum, lepromatous leprosy is characterized by M. leprae proliferation and T cell anergy. Similar to progressive tumor cells, M. leprae escapes immunosurveillance in more severe forms of leprosy. The mechanisms by which M. leprae is able to evade the host immune response involve many, including the alterations of lipid droplets, microRNA, and Schwann cells, and involve the regulation of immune regulators, such as the negative checkpoint regulators CTLA-4, programmed death 1, and V-domain Ig suppressor of T cell activation\u2014important targets in today\u2019s cancer immunotherapies. The means by which tumor cells become able to escape immunosurveillance through negative checkpoint regulators are evidenced by the successes of treatments, such as nivolumab and ipilimumab. Many parallels can be drawn between the immune responses seen in leprosy and cancer. Therefore, the understanding of how M. leprae encourages immune escape during proliferative disease states has potential to add to our understanding of cancer immunotherapy.<\/jats:p>","DOI":"10.1189\/jlb.5ru1215-537rr","type":"journal-article","created":{"date-parts":[[2016,4,23]],"date-time":"2016-04-23T03:13:39Z","timestamp":1461381219000},"page":"47-54","source":"Crossref","is-referenced-by-count":10,"title":["Leprosy as a model to understand cancer immunosurveillance and T cell anergy"],"prefix":"10.1093","volume":"100","author":[{"given":"Andrew J","family":"Park","sequence":"first","affiliation":[{"name":"Geisel School of Medicine, Dartmouth College , Hanover, New Hampshire , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tina","family":"Rendini","sequence":"additional","affiliation":[{"name":"Bellevue Hospital Center, National Hansen\u2019s Disease Program , New York, New York , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"Martiniuk","sequence":"additional","affiliation":[{"name":"iProdynamic Therapeutic , New York, New York , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William R","family":"Levis","sequence":"additional","affiliation":[{"name":"Bellevue Hospital Center, National Hansen\u2019s Disease Program , New York, New York , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2016,4,22]]},"reference":[{"key":"2023011710411724500_B1","doi-asserted-by":"crossref","first-page":"1432","DOI":"10.1126\/science.342.6165.1432","article-title":"Breakthrough of the year 2013. 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