{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T04:31:39Z","timestamp":1791174699821,"version":"4.1.0"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2003,8,1]],"date-time":"2003-08-01T00:00:00Z","timestamp":1059696000000},"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":[[2003,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>In infection with Schistosoma mansoni, parasite eggs precipitate an intrahepatic granulomatous and fibrosing inflammation that is mediated by CD4+ Th cells. Compared with CBA mice, C57BL\/6 mice develop smaller granulomas composed of cells that exhibit reduced proliferative responses to schistosome egg Ags. In the present study, we investigated CD4+ T cell apoptosis as a possible mechanism that could account for this subdued response. We found throughout the course of several infection weeks a markedly higher proportion of apoptotic CD4+ T cells in granulomas from C57BL\/6 mice than in those from CBA mice ex vivo; the apoptosis further increased upon cell cultivation in vitro. Activation-induced cell death or CD8+ T cells failed to account for the enhanced apoptosis as infected Fas-, Fas ligand,- and CD8-deficient mice exhibited similar apoptosis to that seen in wild-type counterparts. However, a strikingly lower IL-2 production by schistosome egg Ag-stimulated C57BL\/6 granuloma and mesenteric lymph node cells suggested the possibility of apoptosis due to growth factor deprivation. Indeed, the CD4+ T cell apoptosis was significantly reversed by addition of rIL-2 in vitro, or by injection of rIL-2 in vivo, which also resulted in significant exacerbation of granulomatous inflammation. These findings indicate that apoptosis by neglect can represent a significant means of controlling CD4+ T cells that mediate the immunopathology in schistosomiasis.<\/jats:p>","DOI":"10.4049\/jimmunol.171.4.1859","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:42:39Z","timestamp":1398022959000},"page":"1859-1867","source":"Crossref","is-referenced-by-count":28,"title":["Apoptosis by Neglect of CD4+ Th Cells in Granulomas: A Novel Effector Mechanism Involved in the Control of Egg-Induced Immunopathology in Murine Schistosomiasis"],"prefix":"10.1093","volume":"171","author":[{"given":"Laura I","family":"Rutitzky","sequence":"first","affiliation":[{"name":"Department of Pathology, Tufts University School of Medicine , Boston, MA 02111"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerardo A","family":"Mirkin","sequence":"additional","affiliation":[{"name":"Department of Pathology, Tufts University School of Medicine , Boston, MA 02111"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miguel J","family":"Stadecker","sequence":"additional","affiliation":[{"name":"Department of Pathology, Tufts University School of Medicine , Boston, MA 02111"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,8,15]]},"reference":[{"key":"2026020210252289200_R1","first-page":"583","volume-title":"Infect. 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