{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T15:07:09Z","timestamp":1774969629963,"version":"3.50.1"},"reference-count":45,"publisher":"Wiley","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"name":"Fondo Nacional de Investigaci\u00f3n y tecnolog\u00eda","award":["11110304"],"award-info":[{"award-number":["11110304"]}]},{"name":"Fondo Nacional de Investigaci\u00f3n y tecnolog\u00eda","award":["020743IB\/021043IB"],"award-info":[{"award-number":["020743IB\/021043IB"]}]},{"name":"Direcci\u00f3n de Investigaciones Cient\u00edficas y Tecnol\u00f3gicas","award":["11110304"],"award-info":[{"award-number":["11110304"]}]},{"name":"Direcci\u00f3n de Investigaciones Cient\u00edficas y Tecnol\u00f3gicas","award":["020743IB\/021043IB"],"award-info":[{"award-number":["020743IB\/021043IB"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2013]]},"abstract":"<jats:p><jats:italic>Neisseria gonorrhoeae<\/jats:italic>is the etiological agent of gonorrhoea, which is a sexually transmitted disease widespread throughout the world.<jats:italic>N. gonorrhoeae<\/jats:italic>does not improve immune response in patients with reinfection, suggesting that gonococcus displays several mechanisms to evade immune response and survive in the host.<jats:italic>N. gonorrhoeae<\/jats:italic>is able to suppress the protective immune response at different levels, such as B and T lymphocytes and dendritic cells. In this study, we determined whether<jats:italic>N. gonorrhoeae<\/jats:italic>directly conditions the phenotype of RAW 264.7 murine macrophage cell line and its response. We established that gonococcus was effectively phagocytosed by the RAW 264.7 cells and upregulates production of immunoregulatory cytokines (IL-10 and TGF-<jats:italic>\u03b2<\/jats:italic>1) but not the production of proinflammatory cytokine TNF-<jats:italic>\u03b1<\/jats:italic>, indicating that gonococcus induces a shift towards anti-inflammatory cytokine production. Moreover,<jats:italic>N. gonorrhoeae<\/jats:italic>did not induce significant upregulation of costimulatory CD86 and MHC class II molecules. We also showed that<jats:italic>N. gonorrhoeae<\/jats:italic>infected macrophage cell line fails to elicit proliferative CD4+ response. This implies that macrophage that can phagocytose gonococcus do not display proper antigen-presenting functions. These results indicate that<jats:italic>N. gonorrhoeae<\/jats:italic>induces a tolerogenic phenotype in antigen-presenting cells, which seems to be one of the mechanisms to induce evasion of immune response.<\/jats:p>","DOI":"10.1155\/2013\/127017","type":"journal-article","created":{"date-parts":[[2013,9,25]],"date-time":"2013-09-25T01:24:29Z","timestamp":1380072269000},"page":"1-9","source":"Crossref","is-referenced-by-count":21,"title":["<i>Neisseria gonorrhoeae<\/i>Induces a Tolerogenic Phenotype in Macrophages to Modulate Host Immunity"],"prefix":"10.1155","volume":"2013","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1587-4179","authenticated-orcid":true,"given":"Alejandro","family":"Escobar","sequence":"first","affiliation":[{"name":"Instituto de Investigaci\u00f3n en Ciencias Odontol\u00f3gicas, Facultad de Odontolog\u00eda, Universidad de Chile, 8380492 Santiago, 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