학술논문
T cell-mediated antitumor immune response eliminates skin tumors induced by mouse papillomavirus, MmuPV1.
Document Type
Academic Journal
Author
Joh J; James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA; Department of Medicine, University of Louisville, Louisville, KY, USA. Electronic address: joongho.joh@louisville.edu.; Chilton PM; Christine M. Kleinert Institute for Hand & Microsurgery, 225 Abraham Flexner Way, Suite 850, Louisville, KY, USA.; Wilcher SA; Research Resources Center, 530 South Jackson Street, Louisville, KY, USA.; Zahin M; James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA.; Park J; James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA; Department of Medicine, University of Louisville, Louisville, KY, USA.; Proctor ML; Research Resources Center, 530 South Jackson Street, Louisville, KY, USA.; Ghim SJ; James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA.; Jenson AB; James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA.
Source
Publisher: Elsevier Country of Publication: Netherlands NLM ID: 0370711 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1096-0945 (Electronic) Linking ISSN: 00144800 NLM ISO Abbreviation: Exp Mol Pathol Subsets: MEDLINE
Subject
Language
English
Abstract
Previous studies of naturally occurring mouse papillomavirus (PV) MmuPV1-induced tumors in B6.Cg-Foxn1 nu/nu mice suggest that T cell deficiency is necessary and sufficient for the development of such tumors. To confirm this, MmuPV1-induced tumors were transplanted from T cell-deficient mice into immunocompetent congenic mice. Consequently, the tumors regressed and eventually disappeared. The elimination of MmuPV1-infected skin/tumors in immunocompetent mice was consistent with the induction of antitumor T cell immunity. This was confirmed by adoptive cell experiments using hyperimmune splenocytes collected from graft-recipient mice. In the present study, such splenocytes were injected into T cell-deficient mice infected with MmuPV1, and they eliminated both early-stage and fully formed tumors. We clearly show that anti-tumor T cell immunity activated during tumor regression in immunocompetent mice effectively eliminates tumors developing in T cell-deficient congenic mice. The results corroborate the notion that PV-induced tumors are strongly linked to the immune status of the host, and that PV antigens are major anti-tumor antigens. Successful anti-PV T cell responses should, therefore, lead to effective anti-tumor immune therapy in human PV-infected patients.
(Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)
(Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)