{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T22:58:37Z","timestamp":1777417117849,"version":"3.51.4"},"reference-count":40,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2003,6,2]],"date-time":"2003-06-02T00:00:00Z","timestamp":1054512000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2003,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Although STAT1\u2010dependent signaling mediates biological functions of IFN\u2010\u03b1\/\u03b2 and IFN\u2010\u03b3, recent reports indicate that STAT1\u2010independent IFN signaling also regulates expression of several genes. To determine the roles of STAT1\u2010dependent and \u2010independent IFN signaling in the regulation of immunity during cutaneous leishmaniasis, we studied the course of <jats:italic>Leishmania major<\/jats:italic> infection in resistant C57BL\/6 mice lacking the STAT1 gene. While <jats:italic>L. major<\/jats:italic>\u2010infected STAT1<jats:sup>+\/+<\/jats:sup> mice resolved their lesions, STAT1<jats:sup>\u2013\/\u2013<\/jats:sup> mice developed large lesions containing significantly more parasites. Moreover, the inability of STAT1<jats:sup>\u2013\/\u2013<\/jats:sup> mice to control <jats:italic>L. major<\/jats:italic> infection was due to the lack of Th1 development associated with reduced production of IL\u201012, IFN\u2010\u03b3 and nitric oxide. Although STAT1<jats:sup>\u2013\/\u2013<\/jats:sup> mice produced more IL\u20104 and total IgE than STAT1<jats:sup>+\/+<\/jats:sup> mice later during infection, these differences were not significant. Nevertheless, at these time points lymph node cells from STAT1<jats:sup>\u2013\/\u2013<\/jats:sup> mice produced significantly more IL\u201010. Finally, STAT1<jats:sup>\u2013\/\u2013<\/jats:sup> mice were also susceptible to low dose <jats:italic>L. major<\/jats:italic> infection. Thesefindings demonstrate that STAT1\u2010mediated IFN signaling is indispensable for the development of protective immunity against cutaneous <jats:italic>L. major<\/jats:italic> infection. Moreover, they also suggest that the protective role of STAT1\u2010mediated signaling is due to its ability to induce Th1 development during infection with this parasite.<\/jats:p>","DOI":"10.1002\/eji.200323163","type":"journal-article","created":{"date-parts":[[2003,6,11]],"date-time":"2003-06-11T15:09:57Z","timestamp":1055344197000},"page":"1799-1805","source":"Crossref","is-referenced-by-count":40,"title":["Development of protective immunity against cutaneous leishmaniasis is dependent on STAT1\u2010mediated IFN signaling pathway"],"prefix":"10.1002","volume":"33","author":[{"given":"Lucia\u2004E.","family":"Rosas","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tracy","family":"Keiser","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ryan","family":"Pyles","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joan","family":"Durbin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Abhay\u2004R.","family":"Satoskar","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2003,6,2]]},"reference":[{"key":"e_1_2_6_1_2","doi-asserted-by":"crossref","first-page":"2993","DOI":"10.1242\/jcs.112.18.2993","article-title":"Leishmania species: models of intracellular parasitism.","volume":"112","author":"Alexander J.","year":"1999","journal-title":"J. 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