{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T17:12:43Z","timestamp":1791306763058,"version":"4.3.1"},"reference-count":24,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2003,2,1]],"date-time":"2003-02-01T00:00:00Z","timestamp":1044057600000},"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":[[2003,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Abscess formation associated with intra-abdominal sepsis causes severe morbidity and can be fatal. Previous studies have implicated T cells in the pathogenesis of abscess formation, and we have recently shown that CD4+ T cells activated in vitro by zwitterionic capsular polysaccharides from abscess-inducing bacteria such as Staphylococcus aureus and Bacteroides fragilis initiate this host response when transferred to naive rats. In this study, we show that mice deficient in \u03b1\u03b2TCR-bearing T cells or CD4+ T cells fail to develop abscesses following challenge with B. fragilis or abscess-inducing zwitterionic polysaccharides, compared with CD8\u2212\/\u2212 or wild-type animals. Transfer of CD4+ T cells from wild-type mice to \u03b1\u03b2TCR\u2212\/\u2212 animals reconstituted this ability. The induction of abscesses required T cell costimulation via the CD28-B7 pathway, and T cell transfer experiments with STAT4\u2212\/\u2212 and STAT6\u2212\/\u2212 mice demonstrated that this host response is dependent on STAT4 signaling. Significantly higher levels of IL-17, a proinflammatory cytokine produced almost exclusively by activated CD4+ T cells, were associated with abscess formation in Th2-impaired (STAT6\u2212\/\u2212) mice, while STAT4\u2212\/\u2212 mice had significantly lower levels of this cytokine than control animals. The formation of abscesses was preceded by an increase in the number of activated CD4+ T cells in the peritoneal cavity 24 h following bacterial challenge. Confocal laser-scanning microscopy analysis revealed that CD4+ T cells comprise the abscess wall in these animals and produce IL-17 at this site. Administration of a neutralizing Ab specific for IL-17 prevented abscess formation following bacterial challenge in mice. These data delineate the specific T cell response necessary for the development of intra-abdominal abscesses and underscore the role of IL-17 in this disease process.<\/jats:p>","DOI":"10.4049\/jimmunol.170.4.1958","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T19:49:07Z","timestamp":1398109747000},"page":"1958-1963","source":"Crossref","is-referenced-by-count":203,"title":["CD4+ T Cells Mediate Abscess Formation in Intra-abdominal Sepsis by an IL-17-Dependent Mechanism"],"prefix":"10.1093","volume":"170","author":[{"given":"Doo Ryeon","family":"Chung","sequence":"first","affiliation":[{"name":"Channing Laboratory, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis L","family":"Kasper","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA 02115"},{"name":"Department of Microbiology and Molecular Genetics, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronald J","family":"Panzo","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanuja","family":"Chtinis","sequence":"additional","affiliation":[{"name":"Department of Neurology, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J","family":"Grusby","sequence":"additional","affiliation":[{"name":"School of Public Health, Department of Immunology and Infectious Disease, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed H","family":"Sayegh","sequence":"additional","affiliation":[{"name":"Laboratory of Immunogenetics and Transplantation, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arthur O","family":"Tzianabos","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Department of Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,2,15]]},"reference":[{"key":"2026020210094190900_R1","volume-title":"Anaerobic Microorganisms in Intraabdominal Infections","year":"1974"},{"key":"2026020210094190900_R2","first-page":"1237","volume-title":"N. 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