{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T13:16:19Z","timestamp":1791292579214,"version":"4.1.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2000,1,1]],"date-time":"2000-01-01T00:00:00Z","timestamp":946684800000},"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":[[2000,1,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>TNF-\u03b1 is known to be an important mediator of tissue damage during allograft rejection and graft-vs-host disease (GVHD), but its role in supporting T cell responses to allogeneic Ags is unclear. We have studied this question by comparing normal mice with those lacking the p55 (p55 TNFR\u2212\/\u2212) or p75 (p75 TNFR\u2212\/\u2212) TNF-\u03b1 receptors as donors in well-defined bone marrow transplant (BMT) models. Recipients of p55 TNFR\u2212\/\u2212 cells had significantly reduced mortality and morbidity from GVHD compared with the other two sources of T cells. In vitro, T cells lacking the p55 (but not the p75) TNF-\u03b1 receptor exhibited decreased proliferation and production of Th1 cytokines in MLC. This defect was only partially restored by exogenous IL-2 and affected both CD4+ and CD8+ populations. CD8+ p55 TNFR\u2212\/\u2212 proliferation was impaired independently of IL-2 whereas CTL effector function was impaired in an IL-2-dependent fashion. Inhibition of TNF-\u03b1 with TNFR:Fc in primary MLC also impaired the proliferation and Th1 differentiation of wild-type T cells. BMT mixing experiments demonstrated that the reduced ability of p55 TNFR\u2212\/\u2212 donor cells to induce GVHD was due to the absence of the p55 TNFR on T cells rather than bone marrow cells. These data highlight the importance of TNF-\u03b1 in alloreactive T cell responses and suggest that inhibition of the T cell p55 TNF-\u03b1 receptor may provide an additional useful therapeutic maneuver to inhibit alloreactive T cell responses following bone marrow and solid organ transplantation.<\/jats:p>","DOI":"10.4049\/jimmunol.164.2.656","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:46:15Z","timestamp":1398023175000},"page":"656-663","source":"Crossref","is-referenced-by-count":110,"title":["The p55 TNF-\u03b1 Receptor Plays a Critical Role in T Cell Alloreactivity"],"prefix":"10.1093","volume":"164","author":[{"given":"Geoffrey R","family":"Hill","sequence":"first","affiliation":[{"name":"Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School , Boston, MA 02115"},{"name":"Mater Medical Research Institute , South Brisbane ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takanori","family":"Teshima","sequence":"additional","affiliation":[{"name":"Departments of Internal Medicine and Pediatrics, Bone Marrow Transplant Program, University of Michigan Cancer Center , MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vivienne I","family":"Rebel","sequence":"additional","affiliation":[{"name":"Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oleg I","family":"Krijanovski","sequence":"additional","affiliation":[{"name":"Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenneth R","family":"Cooke","sequence":"additional","affiliation":[{"name":"Departments of Internal Medicine and Pediatrics, Bone Marrow Transplant Program, University of Michigan Cancer Center , MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yani S","family":"Brinson","sequence":"additional","affiliation":[{"name":"Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James L M","family":"Ferrara","sequence":"additional","affiliation":[{"name":"Departments of Internal Medicine and Pediatrics, Bone Marrow Transplant Program, University of Michigan Cancer Center , MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2000,1,15]]},"reference":[{"key":"2026020213183220600_R1","first-page":"959","volume-title":"Cell","year":"1994"},{"key":"2026020213183220600_R2","first-page":"2830","volume-title":"Proc. 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