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Article: CD28 is not required for rejection of unmanipulated syngeneic and autologous tumors

TitleCD28 is not required for rejection of unmanipulated syngeneic and autologous tumors
Authors
KeywordsCD28
Tumor rejection
B7
Issue Date1997
Citation
European Journal of Immunology, 1997, v. 27, n. 8, p. 1988-1993 How to Cite?
AbstractTo gain a better understanding of the requirement of CD28 co-stimulation in different types of T cell-dependent tumor rejection responses, we performed a series of syngeneic and autologous tumor rejection experiments on CD28 knockout mice. In a preimmunization-challenge model, virally-induced ALC lymphoma and methylcholanthrene induced MC57X fibrosarcoma transplants were rejected similarly by syngeneic CD28 knockout and immunocompetent controls. ALC-specific cytotoxic T lymphocytes (CTL) and MC57X-specific tumor necrosis factor (TNF) release were induced in CD28 knockouts, although at a reduced level in the latter case. Secondly, the spontaneous regression of Moloney murine sarcoma virus (MMSV)-induced primary tumors in the autologous hosts occurred equally in CD28 knockouts and in immunocompetent control mice. A comparable virus-specific CTL response was generated in both, as revealed in cytolytic assays against RBL-5 targets. Thirdly, the spontaneous rejection of the B7-transfected EL-4 lymphoma by immunocompetent hosts was abrogated in CD28 knockout mice, since more than 82% CD28 knockouts developed tumors after inoculation with B7-transfected EL-4 cells. Our results therefore show that CD28 co-stimulatory molecules are not required for the rejection of unmanipulated syngeneic tumors in hyperimmunized hosts and the regression of MMSV-induced sarcoma in autochthonous hosts.
Persistent Identifierhttp://hdl.handle.net/10722/291394
ISSN
2023 Impact Factor: 4.5
2023 SCImago Journal Rankings: 1.627
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWen, Tao-
dc.contributor.authorKono, Koji-
dc.contributor.authorShahinian, Arda-
dc.contributor.authorKiessling, Rolf-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorKlein, George-
dc.date.accessioned2020-11-17T14:54:16Z-
dc.date.available2020-11-17T14:54:16Z-
dc.date.issued1997-
dc.identifier.citationEuropean Journal of Immunology, 1997, v. 27, n. 8, p. 1988-1993-
dc.identifier.issn0014-2980-
dc.identifier.urihttp://hdl.handle.net/10722/291394-
dc.description.abstractTo gain a better understanding of the requirement of CD28 co-stimulation in different types of T cell-dependent tumor rejection responses, we performed a series of syngeneic and autologous tumor rejection experiments on CD28 knockout mice. In a preimmunization-challenge model, virally-induced ALC lymphoma and methylcholanthrene induced MC57X fibrosarcoma transplants were rejected similarly by syngeneic CD28 knockout and immunocompetent controls. ALC-specific cytotoxic T lymphocytes (CTL) and MC57X-specific tumor necrosis factor (TNF) release were induced in CD28 knockouts, although at a reduced level in the latter case. Secondly, the spontaneous regression of Moloney murine sarcoma virus (MMSV)-induced primary tumors in the autologous hosts occurred equally in CD28 knockouts and in immunocompetent control mice. A comparable virus-specific CTL response was generated in both, as revealed in cytolytic assays against RBL-5 targets. Thirdly, the spontaneous rejection of the B7-transfected EL-4 lymphoma by immunocompetent hosts was abrogated in CD28 knockout mice, since more than 82% CD28 knockouts developed tumors after inoculation with B7-transfected EL-4 cells. Our results therefore show that CD28 co-stimulatory molecules are not required for the rejection of unmanipulated syngeneic tumors in hyperimmunized hosts and the regression of MMSV-induced sarcoma in autochthonous hosts.-
dc.languageeng-
dc.relation.ispartofEuropean Journal of Immunology-
dc.subjectCD28-
dc.subjectTumor rejection-
dc.subjectB7-
dc.titleCD28 is not required for rejection of unmanipulated syngeneic and autologous tumors-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/eji.1830270824-
dc.identifier.pmid9295036-
dc.identifier.scopuseid_2-s2.0-0030738298-
dc.identifier.volume27-
dc.identifier.issue8-
dc.identifier.spage1988-
dc.identifier.epage1993-
dc.identifier.isiWOS:A1997XQ08000023-
dc.identifier.issnl0014-2980-

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