Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruzi
Autor(a) principal: | |
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Data de Publicação: | 1992 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1084/jem.175.1.29 http://hdl.handle.net/11449/230874 |
Resumo: | The contribution of autoimmunity in the genesis of chronic Chagas' heart pathology is not dear. In the present study, we show that: (a) BALB/c mice chronically infected with Trypanosoma cruzi reject syngeneic newborn hearts; (b) in vivo treatment with anti-CD4 but not anti-CD8 monodonal antibodies (mAbs) abrogates rejection; (c) CD4+ T calls from chronically infected mice proliferate in vitro to syngeneic myocardium antigens and induce heart graft destruction when injected in situ; (d) anti-CD4 treatment of chronically infected mice establishes long-term tolerance to syngeneic heart grafts; and (e) the state of tolerance is related to in vitro and in vivo unresponsiveness of the CD4+ T cells. These findings allow us to suggest that autoimmunity is the major mechanism implicated in the rejection of syngeneic heart tissues grafted into the pinna of the ear of mice chronically infected with T. cruzi. The similarity of the lesions to those found in humans suggests that autoimmunity is involved in the pathogenesis of chagasic cardiomyopathy in humans. Moreover, this could imply therapeutic strategies by reestablishing long-term tissue-specific tolerance with anti-CD4 mAb treatment, mediating anergy, or deleting the responder CD4+ T cells to heart tissue antigens. © 1992, Rockefeller University Press., All rights reserved. |
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Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruziThe contribution of autoimmunity in the genesis of chronic Chagas' heart pathology is not dear. In the present study, we show that: (a) BALB/c mice chronically infected with Trypanosoma cruzi reject syngeneic newborn hearts; (b) in vivo treatment with anti-CD4 but not anti-CD8 monodonal antibodies (mAbs) abrogates rejection; (c) CD4+ T calls from chronically infected mice proliferate in vitro to syngeneic myocardium antigens and induce heart graft destruction when injected in situ; (d) anti-CD4 treatment of chronically infected mice establishes long-term tolerance to syngeneic heart grafts; and (e) the state of tolerance is related to in vitro and in vivo unresponsiveness of the CD4+ T cells. These findings allow us to suggest that autoimmunity is the major mechanism implicated in the rejection of syngeneic heart tissues grafted into the pinna of the ear of mice chronically infected with T. cruzi. The similarity of the lesions to those found in humans suggests that autoimmunity is involved in the pathogenesis of chagasic cardiomyopathy in humans. Moreover, this could imply therapeutic strategies by reestablishing long-term tissue-specific tolerance with anti-CD4 mAb treatment, mediating anergy, or deleting the responder CD4+ T cells to heart tissue antigens. © 1992, Rockefeller University Press., All rights reserved.Evandro Chagas Hospital Instituto Oswaldo Cruz, Rio de Janeiro, 20010Department of Pathology Faculty of Medicine of Ribeirão Preto University of São Paulo, Ribeirão Preto, 14049Department of Surgery Faculty of Veterinary Medicine Unesp, Jaboticabal, 14870Department of Immunology Faculty of Medicine of Ribeirão Preto University of São Paulo, Ribeirão Preto, 14049Department of Immunology Instituto Oswaldo Cruz, Rio de Janeiro, 20010Department of Surgery Faculty of Veterinary Medicine Unesp, Jaboticabal, 14870Instituto Oswaldo CruzUniversidade de São Paulo (USP)Universidade Estadual Paulista (UNESP)Santos, R. Ribeiro DosRossi, Marcos A.Laus, J. L. [UNESP]Silva, J. SantanaSavino, WilsonMengel, José2022-04-29T08:42:26Z2022-04-29T08:42:26Z1992-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article29-39http://dx.doi.org/10.1084/jem.175.1.29Journal of Experimental Medicine, v. 175, n. 1, p. 29-39, 1992.1540-95380022-1007http://hdl.handle.net/11449/23087410.1084/jem.175.1.292-s2.0-0026593438Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengJournal of Experimental Medicineinfo:eu-repo/semantics/openAccess2022-04-29T08:42:26Zoai:repositorio.unesp.br:11449/230874Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T16:51:51.545996Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruzi |
title |
Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruzi |
spellingShingle |
Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruzi Santos, R. Ribeiro Dos |
title_short |
Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruzi |
title_full |
Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruzi |
title_fullStr |
Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruzi |
title_full_unstemmed |
Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruzi |
title_sort |
Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with trypanosoma cruzi |
author |
Santos, R. Ribeiro Dos |
author_facet |
Santos, R. Ribeiro Dos Rossi, Marcos A. Laus, J. L. [UNESP] Silva, J. Santana Savino, Wilson Mengel, José |
author_role |
author |
author2 |
Rossi, Marcos A. Laus, J. L. [UNESP] Silva, J. Santana Savino, Wilson Mengel, José |
author2_role |
author author author author author |
dc.contributor.none.fl_str_mv |
Instituto Oswaldo Cruz Universidade de São Paulo (USP) Universidade Estadual Paulista (UNESP) |
dc.contributor.author.fl_str_mv |
Santos, R. Ribeiro Dos Rossi, Marcos A. Laus, J. L. [UNESP] Silva, J. Santana Savino, Wilson Mengel, José |
description |
The contribution of autoimmunity in the genesis of chronic Chagas' heart pathology is not dear. In the present study, we show that: (a) BALB/c mice chronically infected with Trypanosoma cruzi reject syngeneic newborn hearts; (b) in vivo treatment with anti-CD4 but not anti-CD8 monodonal antibodies (mAbs) abrogates rejection; (c) CD4+ T calls from chronically infected mice proliferate in vitro to syngeneic myocardium antigens and induce heart graft destruction when injected in situ; (d) anti-CD4 treatment of chronically infected mice establishes long-term tolerance to syngeneic heart grafts; and (e) the state of tolerance is related to in vitro and in vivo unresponsiveness of the CD4+ T cells. These findings allow us to suggest that autoimmunity is the major mechanism implicated in the rejection of syngeneic heart tissues grafted into the pinna of the ear of mice chronically infected with T. cruzi. The similarity of the lesions to those found in humans suggests that autoimmunity is involved in the pathogenesis of chagasic cardiomyopathy in humans. Moreover, this could imply therapeutic strategies by reestablishing long-term tissue-specific tolerance with anti-CD4 mAb treatment, mediating anergy, or deleting the responder CD4+ T cells to heart tissue antigens. © 1992, Rockefeller University Press., All rights reserved. |
publishDate |
1992 |
dc.date.none.fl_str_mv |
1992-01-01 2022-04-29T08:42:26Z 2022-04-29T08:42:26Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1084/jem.175.1.29 Journal of Experimental Medicine, v. 175, n. 1, p. 29-39, 1992. 1540-9538 0022-1007 http://hdl.handle.net/11449/230874 10.1084/jem.175.1.29 2-s2.0-0026593438 |
url |
http://dx.doi.org/10.1084/jem.175.1.29 http://hdl.handle.net/11449/230874 |
identifier_str_mv |
Journal of Experimental Medicine, v. 175, n. 1, p. 29-39, 1992. 1540-9538 0022-1007 10.1084/jem.175.1.29 2-s2.0-0026593438 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Journal of Experimental Medicine |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
29-39 |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
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1808128712305016832 |