Intercellular adhesion molecule 1 deficiency leads to impaired recruitment of T lymphocytes and enhanced host susceptibility to infection with Trypanosoma cruzi

dc.creatorMichailowsky, Vladimir
dc.creatorCeles, Mara R. N.
dc.creatorMarino, Ana P.
dc.creatorSilva, Andréa A.
dc.creatorVieira, Leda Q.
dc.creatorRossi, Marcos A.
dc.creatorGazzinelli, Ricardo T.
dc.creatorLannes-Vieira, Joseli
dc.creatorSilva, João S.
dc.date2020-03-25T19:40:40Z
dc.date2020-03-25T19:40:40Z
dc.date2004
dc.date.accessioned2023-09-26T22:28:13Z
dc.date.available2023-09-26T22:28:13Z
dc.identifierMICHAILOWSKY, Vladimir et al. Intercellular Adhesion Molecule 1 Deficiency Leads to Impaired Recruitment of T Lymphocytes and Enhanced Host Susceptibility to Infection with Trypanosoma cruzi. Journal of Immunology, v. 173, p. 463-470, 2020.
dc.identifier0022-1767
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/40517
dc.identifier10.4049/jimmunol.173.1.463
dc.identifier1550-6606
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8879642
dc.descriptionArtigo encontra-se em acesso aberto pelo editor - https://www.jimmunol.org/content/173/1/463.long
dc.descriptionIn this study, we investigated the involvement of Th1 cytokines in the expression of cell adhesion molecules (CAM) and recruitment of inflammatory cells to the heart of mice infected with Trypanosoma cruzi. Our results show that endogenously produced IFN-gamma is essential to induce optimal expression of VCAM-1 and ICAM-1 on the cardiac vascular endothelium of infected mice. Furthermore, the influx of inflammatory cells into the cardiac tissue was impaired in Th1 cytokine-deficient infected mice, paralleling the intensity of VCAM-1 and ICAM-1 expression on the vascular endothelium. Consistent with the importance of ICAM-1 in host resistance, ICAM-1 knockout (KO) mice were highly susceptible to T. cruzi infection, as assessed by mortality rate, parasitemia, and heart tissue parasitism. The enhanced parasitism was associated with a decrease in the numbers of CD4(+) and CD8(+) T lymphocytes in the heart tissue of ICAM-1 KO mice. Additionally, ICAM-1 KO mice mounted an unimpaired IFN-gamma response and IFN-gamma-dependent production of reactive nitrogen intermediates and parasite- specific IgG2a. Supporting the participation of ICAM-1 in cell migration during T. cruzi infection, the entrance of adoptively transferred PBL from T. cruzi-infected wild-type C57BL/6 mice into the cardiac tissue of ICAM-1 KO mice was significantly abrogated. Therefore, we favor the hypothesis that ICAM-1 plays a crucial role in T lymphocyte recruitment to the cardiac tissue and host susceptibility during T. cruzi infection.
dc.description2022-01-01
dc.formatapplication/pdf
dc.languageeng
dc.publisherThe American Association of Immunologists
dc.rightsrestricted access
dc.subjectTrypanosoma cruzi
dc.subjectInfecção
dc.subjectLinfócitos T
dc.subjectMolécula de adesão intercelular
dc.subjectTrypanosoma cruzi
dc.subjectIntercellular adhesion molecule
dc.subjectInfection
dc.subjectT lymphocytes
dc.titleIntercellular adhesion molecule 1 deficiency leads to impaired recruitment of T lymphocytes and enhanced host susceptibility to infection with Trypanosoma cruzi
dc.typeArticle


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