부산대학교 도서관

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1365-2567.2007.02677.x Byline: Fabiola Cardillo (1), Edilberto Postol (2), Jorge Nihei (1), Luiz S. Aroeira (3), Auro Nomizo (4), Jose Mengel (1) Keywords: Trypanosoma cruzi; B cells; IFN-[gamma]; memory; CD8 Abstract: Summary In this study, we have evaluated the production of pro- and anti-inflammatory cytokines and the formation of central and effector memory T cells in mice lacking mature B cells (muMT KO). The results show that Trypanosoma cruzi infection in C57Bl/6m[mu] MT KO mice is intensified in relation to control mice and this exacerbation is related to low levels of inflammatory cytokines produced during the acute infection and the lower numbers of central and effector memory CD4.sup.+ and CD8.sup.+ T cells generated during the acute phase of the infection. In addition, a marked reduction in the CD8.sup.+ T-cell subpopulation was observed in muMT KO infected mice. In agreement to this, the degree of tissue parasitism was increased in muMT mice and the tissue inflammatory response was much less intense in the acute phase of the infection, consistent with a deficit in the generation of effector T cells. Flow cytometry analysis of the skeletal muscle inflammatory infiltrate showed a predominance of CD8.sup.+ CD45Rb low in B-cell-sufficient C57Bl/6 mice, whereas the preponderant cell type in muMT KO skeletal muscle inflammatory infiltrate was CD4.sup.+ T cells. In addition, CD8.sup.+ T cells found in skeletal muscle from muMT KO infected mice were less activated than in control B-cell sufficient infected mice. These results suggest that B cells may participate in the generation of effector/memory T cells. In addition and more importantly, B cells were crucial in the maintenance of central and effector memory CD8.sup.+ T cell, as well as the determination of the T cell cytokine functional pattern, and they may therefore account for critical aspects of the resistance to intracellular pathogens, such as T. cruzi. Author Affiliation: (1)Cellular Immunology, Autoimmunity and Experimental Chagas Disease Laboratory, Oswaldo Cruz Foundation, Goncalo Moniz Research Center, Salvador, Bahia, Brazil (2)Immunology Laboratory, Heart Institute (INCOR), University of Sao Paulo, Sao Paulo, SP, Brazil (3)Unidad de Investigacion Hospital La Paz, Madrid, Spain (4)Department of Clinical Analysis, Toxicology and Bromatology, Faculty of Pharmaceutical Sciences of Ribeirao Preto, University of Sao Paulo, Brazil Article History: Received 30 January 2007; revised 11 June 2007; accepted 11 June 2007. Article note: Dr J. Mengel, Oswaldo Cruz Foundation, Centro de Pesquisas Goncalo Moniz. R. Waldemar Falcao 121, 40296-710, Candeal, Salvador, Bahia, Brazil., Email: jomengel@cpqgm.fiocruz.br, Senior author: Fabiola Cardillo, email: cardillo@cpqgm.fiocruz.br