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Specific Remodeling of Splenic Architecture by Cytomegalovirus

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Specific Remodeling of Splenic Architecture by Cytomegalovirus
Id. 5313865
Idioma inglés
Titulo Specific Remodeling of Splenic Architecture by Cytomegalovirus
Autor(es) Benedict, Chris A
De Trez, Carl
Schneider, Kirsten
Ha, Sukwon
Patterson, Ginelle
Ware, Carl F
Localización http://www.pubmedcentral.gov/articlerender.fcgi?artid=1386719
Versión 1.0
Estado Final
Descripción Efficient immune defenses are facilitated by the organized microarchitecture of lymphoid organs, and this organization is regulated by the compartmentalized expression of lymphoid tissue chemokines. Mouse cytomegalovirus (MCMV) infection induces significant remodeling of splenic microarchitecture, including loss of marginal zone macrophage populations and dissolution of T and B cell compartmentalization. MCMV preferentially infected the splenic stroma, targeting endothelial cells (EC) as revealed using MCMV-expressing green fluorescent protein. MCMV infection caused a specific, but transient transcriptional suppression of secondary lymphoid chemokine (CCL21). The loss of CCL21 was associated with the failure of T lymphocytes to locate within the T cell zone, although trafficking to the spleen was unaltered. Expression of CCL21 in lymphotoxin (LT)-?–deficient mice is dramatically reduced, however MCMV infection further reduced CCL21 levels, suggesting that viral modulation of CCL21 was independent of LT? signaling. Activation of LT?-receptor signaling with an agonistic antibody partially restored CCL21 mRNA expression and redirected transferred T cells to the splenic T cell zone in MCMV-infected mice. These results indicate that virus-induced alterations in lymphoid tissues can occur through an LT-independent modulation of chemokine transcription, and targeting of the LT cytokine system can counteract lymphoid tissue remodeling by MCMV.
Palabras clave Research Article
Tipo de recurso Text
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Copyright
Copyright: © 2006 Benedict et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Fecha de contribución 01-dic-2006
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