Trypanosoma cruzi calreticulin: A possible role in Chagas' disease autoimmunity

Carolina Hager Ribeiro, Nandy C. López, Galia A. Ramírez, Carolina E. Valck, María Carmen Molina, Lorena Aguilar, Margarita Rodríguez, Ismael Maldonado, Ramón Martínez, Carlos González, Rodrigo Troncoso, Sergio Lavandero, Alexandre R. Gingras, Wilhelm Schwaeble, Arturo Ferreira

Resultado de la investigación: Article

26 Citas (Scopus)

Resumen

Trypanosoma cruzi (T. cruzi) is the causative agent of Chagas' disease, an endemic and chronic illness that affects 18 million people in Latin America. The mechanisms underlying its pathogenesis are controversial. There is a growing body of evidence supporting the view that T. cruzi infection elicits severe autoimmune responses in the host, which significantly contribute to the pathogenesis of Chagas' disease, and several recent studies have reported the presence of autoantibodies and effector T lymphocytes against parasite and self antigens in infected patients and experimentally infected animals. T. cruzi calreticulin (TcCRT) is a 45 kDa protein, immunogenic in humans, rabbits and mice. It has a high degree of homology with human (HuCRT) and mouse calreticulin (MoCRT), which would explain why an immune response to TcCRT could contribute to autoimmune reactions in Chagas' disease. Anti-TcCRT antibodies generated in A/J mice immunized with recombinant TcCRT (rTcCRT) reacted with rHuCRT and bound to neonatal and adult isogenic cardiomyocytes cultured in vitro. Interestingly, histological alterations, such as edema formation and cell infiltrates, which include CD3+ cells, were detected in heart sections from immunized animals. Therefore, in rTcCRT-immunized mice, an autoimmune reaction against host CRT, paralleled by histological cardiac alterations, suggests a role of the parasite molecule in the induction of immunologically mediated heart tissue damage. The data presented here propose that TcCRT participates in the induction of cardiac autoimmunity in Chagas' disease.

Idioma originalEnglish
Páginas (desde-hasta)1092-1099
Número de páginas8
PublicaciónMolecular Immunology
Volumen46
N.º6
DOI
EstadoPublished - 1 mar 2009

Huella dactilar

Calreticulin
Chagas Disease
Trypanosoma cruzi
Autoimmunity
Parasites
Latin America
Autoantigens
Cardiac Myocytes
Autoantibodies
Edema
Chronic Disease
Rabbits
T-Lymphocytes
Antibodies
Infection

ASJC Scopus subject areas

  • Immunology
  • Molecular Biology

Citar esto

Ribeiro, C. H., López, N. C., Ramírez, G. A., Valck, C. E., Molina, M. C., Aguilar, L., ... Ferreira, A. (2009). Trypanosoma cruzi calreticulin: A possible role in Chagas' disease autoimmunity. Molecular Immunology, 46(6), 1092-1099. https://doi.org/10.1016/j.molimm.2008.10.034
Ribeiro, Carolina Hager ; López, Nandy C. ; Ramírez, Galia A. ; Valck, Carolina E. ; Molina, María Carmen ; Aguilar, Lorena ; Rodríguez, Margarita ; Maldonado, Ismael ; Martínez, Ramón ; González, Carlos ; Troncoso, Rodrigo ; Lavandero, Sergio ; Gingras, Alexandre R. ; Schwaeble, Wilhelm ; Ferreira, Arturo. / Trypanosoma cruzi calreticulin : A possible role in Chagas' disease autoimmunity. En: Molecular Immunology. 2009 ; Vol. 46, N.º 6. pp. 1092-1099.
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abstract = "Trypanosoma cruzi (T. cruzi) is the causative agent of Chagas' disease, an endemic and chronic illness that affects 18 million people in Latin America. The mechanisms underlying its pathogenesis are controversial. There is a growing body of evidence supporting the view that T. cruzi infection elicits severe autoimmune responses in the host, which significantly contribute to the pathogenesis of Chagas' disease, and several recent studies have reported the presence of autoantibodies and effector T lymphocytes against parasite and self antigens in infected patients and experimentally infected animals. T. cruzi calreticulin (TcCRT) is a 45 kDa protein, immunogenic in humans, rabbits and mice. It has a high degree of homology with human (HuCRT) and mouse calreticulin (MoCRT), which would explain why an immune response to TcCRT could contribute to autoimmune reactions in Chagas' disease. Anti-TcCRT antibodies generated in A/J mice immunized with recombinant TcCRT (rTcCRT) reacted with rHuCRT and bound to neonatal and adult isogenic cardiomyocytes cultured in vitro. Interestingly, histological alterations, such as edema formation and cell infiltrates, which include CD3+ cells, were detected in heart sections from immunized animals. Therefore, in rTcCRT-immunized mice, an autoimmune reaction against host CRT, paralleled by histological cardiac alterations, suggests a role of the parasite molecule in the induction of immunologically mediated heart tissue damage. The data presented here propose that TcCRT participates in the induction of cardiac autoimmunity in Chagas' disease.",
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Ribeiro, CH, López, NC, Ramírez, GA, Valck, CE, Molina, MC, Aguilar, L, Rodríguez, M, Maldonado, I, Martínez, R, González, C, Troncoso, R, Lavandero, S, Gingras, AR, Schwaeble, W & Ferreira, A 2009, 'Trypanosoma cruzi calreticulin: A possible role in Chagas' disease autoimmunity', Molecular Immunology, vol. 46, n.º 6, pp. 1092-1099. https://doi.org/10.1016/j.molimm.2008.10.034

Trypanosoma cruzi calreticulin : A possible role in Chagas' disease autoimmunity. / Ribeiro, Carolina Hager; López, Nandy C.; Ramírez, Galia A.; Valck, Carolina E.; Molina, María Carmen; Aguilar, Lorena; Rodríguez, Margarita; Maldonado, Ismael; Martínez, Ramón; González, Carlos; Troncoso, Rodrigo; Lavandero, Sergio; Gingras, Alexandre R.; Schwaeble, Wilhelm; Ferreira, Arturo.

En: Molecular Immunology, Vol. 46, N.º 6, 01.03.2009, p. 1092-1099.

Resultado de la investigación: Article

TY - JOUR

T1 - Trypanosoma cruzi calreticulin

T2 - A possible role in Chagas' disease autoimmunity

AU - Ribeiro, Carolina Hager

AU - López, Nandy C.

AU - Ramírez, Galia A.

AU - Valck, Carolina E.

AU - Molina, María Carmen

AU - Aguilar, Lorena

AU - Rodríguez, Margarita

AU - Maldonado, Ismael

AU - Martínez, Ramón

AU - González, Carlos

AU - Troncoso, Rodrigo

AU - Lavandero, Sergio

AU - Gingras, Alexandre R.

AU - Schwaeble, Wilhelm

AU - Ferreira, Arturo

PY - 2009/3/1

Y1 - 2009/3/1

N2 - Trypanosoma cruzi (T. cruzi) is the causative agent of Chagas' disease, an endemic and chronic illness that affects 18 million people in Latin America. The mechanisms underlying its pathogenesis are controversial. There is a growing body of evidence supporting the view that T. cruzi infection elicits severe autoimmune responses in the host, which significantly contribute to the pathogenesis of Chagas' disease, and several recent studies have reported the presence of autoantibodies and effector T lymphocytes against parasite and self antigens in infected patients and experimentally infected animals. T. cruzi calreticulin (TcCRT) is a 45 kDa protein, immunogenic in humans, rabbits and mice. It has a high degree of homology with human (HuCRT) and mouse calreticulin (MoCRT), which would explain why an immune response to TcCRT could contribute to autoimmune reactions in Chagas' disease. Anti-TcCRT antibodies generated in A/J mice immunized with recombinant TcCRT (rTcCRT) reacted with rHuCRT and bound to neonatal and adult isogenic cardiomyocytes cultured in vitro. Interestingly, histological alterations, such as edema formation and cell infiltrates, which include CD3+ cells, were detected in heart sections from immunized animals. Therefore, in rTcCRT-immunized mice, an autoimmune reaction against host CRT, paralleled by histological cardiac alterations, suggests a role of the parasite molecule in the induction of immunologically mediated heart tissue damage. The data presented here propose that TcCRT participates in the induction of cardiac autoimmunity in Chagas' disease.

AB - Trypanosoma cruzi (T. cruzi) is the causative agent of Chagas' disease, an endemic and chronic illness that affects 18 million people in Latin America. The mechanisms underlying its pathogenesis are controversial. There is a growing body of evidence supporting the view that T. cruzi infection elicits severe autoimmune responses in the host, which significantly contribute to the pathogenesis of Chagas' disease, and several recent studies have reported the presence of autoantibodies and effector T lymphocytes against parasite and self antigens in infected patients and experimentally infected animals. T. cruzi calreticulin (TcCRT) is a 45 kDa protein, immunogenic in humans, rabbits and mice. It has a high degree of homology with human (HuCRT) and mouse calreticulin (MoCRT), which would explain why an immune response to TcCRT could contribute to autoimmune reactions in Chagas' disease. Anti-TcCRT antibodies generated in A/J mice immunized with recombinant TcCRT (rTcCRT) reacted with rHuCRT and bound to neonatal and adult isogenic cardiomyocytes cultured in vitro. Interestingly, histological alterations, such as edema formation and cell infiltrates, which include CD3+ cells, were detected in heart sections from immunized animals. Therefore, in rTcCRT-immunized mice, an autoimmune reaction against host CRT, paralleled by histological cardiac alterations, suggests a role of the parasite molecule in the induction of immunologically mediated heart tissue damage. The data presented here propose that TcCRT participates in the induction of cardiac autoimmunity in Chagas' disease.

KW - Autoimmunity

KW - Calreticulin

KW - Chagas' disease

KW - Trypanosoma cruzi

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DO - 10.1016/j.molimm.2008.10.034

M3 - Article

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AN - SCOPUS:60949092870

VL - 46

SP - 1092

EP - 1099

JO - Molecular Immunology

JF - Molecular Immunology

SN - 0161-5890

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Ribeiro CH, López NC, Ramírez GA, Valck CE, Molina MC, Aguilar L y otros. Trypanosoma cruzi calreticulin: A possible role in Chagas' disease autoimmunity. Molecular Immunology. 2009 mar 1;46(6):1092-1099. https://doi.org/10.1016/j.molimm.2008.10.034