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In this study, we show that in the absence of a protective NK cell response, murine CMV causes destruction of splenic white and red pulp pulp areas in the first few days of infection. Destruction of T zone stroma is associated with almost complete loss of dendritic cells and T cells. We provide evidence that the virus replicates in red and white pulp stroma in vivo and in vitro. Control of white pulp viral replication is associated with migration of murine CMV-specific activated NK cells to white pulp areas, where they associate directly with podoplanin-expressing T zone stromal cells. Our data explain how NK cells protect the lymphoid-rich white pulp areas from CMV, allowing protective adaptive T cell-dependent immune responses to develop, and how this mechanism might break down in immunocompromised patients.

Original publication




Journal article


J immunol

Publication Date





6768 - 6776


Animals, Antigens, Ly, Chemokine CXCL10, Chemokine CXCL11, Chemotaxis, Leukocyte, Flow Cytometry, Herpesviridae Infections, Immunohistochemistry, Killer Cells, Natural, Lasers, Lectins, C-Type, Mice, Microdissection, Microscopy, Confocal, Muromegalovirus, NK Cell Lectin-Like Receptor Subfamily A, Receptors, CXCR3, Receptors, NK Cell Lectin-Like, Reverse Transcriptase Polymerase Chain Reaction, Spleen, T-Lymphocytes