{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T00:40:49Z","timestamp":1791852049248,"version":"4.3.4"},"reference-count":88,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2017,10,1]],"date-time":"2017-10-01T00:00:00Z","timestamp":1506816000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"N\/A"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Clin Vaccine Immunol"],"published-print":{"date-parts":[[2017,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:named-content content-type=\"genus-species\">Chlamydia trachomatis<\/jats:named-content>\n                    is an obligate intracellular bacterium whose only natural host is humans. Although presenting as asymptomatic in most women, genital tract chlamydial infections are a leading cause of pelvic inflammatory disease, tubal factor infertility, and ectopic pregnancy.\n                    <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n                    has evolved successful mechanisms to avoid destruction by autophagy and the host immune system and persist within host epithelial cells. The intracellular form of this organism, the reticulate body, can enter into a persistent nonreplicative but viable state under unfavorable conditions. The infectious form of the organism, the elementary body, is again generated when the immune attack subsides. In its persistent form,\n                    <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n                    ceases to produce its major structural and membrane components, but synthesis of its 60-kDa heat shock protein (hsp60) is greatly upregulated and released from the cell. The immune response to hsp60, perhaps exacerbated by repeated cycles of productive infection and persistence, may promote damage to fallopian tube epithelial cells, scar formation, and tubal occlusion. The chlamydial and human hsp60 proteins are very similar, and hsp60 is one of the first proteins produced by newly formed embryos. Thus, the development of immunity to epitopes in the chlamydial hsp60 that are also present in the corresponding human hsp60 may increase susceptibility to pregnancy failure in infected women. Delineation of host factors that increase the likelihood that\n                    <jats:named-content content-type=\"genus-species\">C. trachomatis<\/jats:named-content>\n                    will avoid immune destruction and survive within host epithelial cells and utilization of this knowledge to design individualized preventative and treatment protocols are needed to more effectively combat infections by this persistent pathogen.\n                  <\/jats:p>","DOI":"10.1128\/cvi.00203-17","type":"journal-article","created":{"date-parts":[[2017,8,23]],"date-time":"2017-08-23T20:40:24Z","timestamp":1503520824000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":175,"title":["Chlamydia trachomatis: the Persistent Pathogen"],"prefix":"10.1128","volume":"24","author":[{"given":"Steven S.","family":"Witkin","sequence":"first","affiliation":[{"name":"Division of Immunology and Infectious Diseases, Department of Obstetrics and Gynecology, Weill Cornell Medicine, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evelyn","family":"Minis","sequence":"additional","affiliation":[{"name":"Division of Immunology and Infectious Diseases, Department of Obstetrics and Gynecology, Weill Cornell Medicine, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aikaterini","family":"Athanasiou","sequence":"additional","affiliation":[{"name":"Division of Immunology and Infectious Diseases, Department of Obstetrics and Gynecology, Weill Cornell Medicine, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Leizer","sequence":"additional","affiliation":[{"name":"Division of Immunology and Infectious Diseases, Department of Obstetrics and Gynecology, Weill Cornell Medicine, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iara M.","family":"Linhares","sequence":"additional","affiliation":[{"name":"Division of Immunology and Infectious Diseases, Department of Obstetrics and Gynecology, Weill Cornell Medicine, New York, New York, USA"},{"name":"Department of Gynecology and Obstetrics, University of S\u00e3o Paulo Medical School, S\u00e3o Paulo, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1086\/652402"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/1574-6976.12059"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro.2016.30"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a010256"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.micinf.2015.08.004"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.femsre.2005.03.002"},{"key":"e_1_3_1_8_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0703218104"},{"key":"e_1_3_1_9_2","doi-asserted-by":"publisher","DOI":"10.3201\/eid0204.960406"},{"key":"e_1_3_1_10_2","doi-asserted-by":"publisher","DOI":"10.1086\/652392"},{"key":"e_1_3_1_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2011.10.026"},{"key":"e_1_3_1_12_2","doi-asserted-by":"publisher","DOI":"10.4161\/auto.5778"},{"key":"e_1_3_1_13_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.72.8.4751-4762.2004"},{"key":"e_1_3_1_14_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-6968.2009.01494.x"},{"key":"e_1_3_1_15_2","doi-asserted-by":"publisher","DOI":"10.4161\/auto.22482"},{"key":"e_1_3_1_16_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0004588"},{"key":"e_1_3_1_17_2","doi-asserted-by":"publisher","DOI":"10.4161\/auto.7.8.15597"},{"key":"e_1_3_1_18_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jri.2009.07.013"},{"key":"e_1_3_1_19_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.3.1435"},{"key":"e_1_3_1_20_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-5822.2006.00686.x"},{"key":"e_1_3_1_21_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.00105-13"},{"key":"e_1_3_1_22_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00129-17"},{"key":"e_1_3_1_23_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.193.8.935"},{"key":"e_1_3_1_24_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.tim.2009.07.007"},{"key":"e_1_3_1_25_2","doi-asserted-by":"crossref","first-page":"4491","DOI":"10.1128\/IAI.66.9.4491-4495.1998","article-title":"Beta interferon is produced by Chlamydia trachomatis-infected fibroblast-like synoviocytes and inhibits gamma interferon-induced HLA-DR expression","volume":"66","author":"Rodel J","year":"1998","unstructured":"Rodel J GrohAVogelsangHLehmannMHartmannMStraubeE. 1998. 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