Differential requirement for CD28 and CD80/86 pathways of costimulation in the long-term control of murine gammaherpesvirus-68.

The costimulatory molecules CD80 and CD86 (B7-1 and B7-2) are upregulated on mature antigen-presenting cells and interact with positive and negative regulators of CD8 T cell function, CD28 and CD152 (CTLA4) respectively. In this study, we examined the role of CD80 and CD86 in the immune response to murine gammaherpesvirus-68 (MHV-68) using CD80/86-/- mice. As we had previously shown that CD28 (the only known activating receptor for CD80 and 86) is not essential for long-term control of MHV-68, we predicted that CD80 and 86 would also be dispensable for an effective response to this virus.

Protein kinase C theta is not essential for T-cell-mediated clearance of murine gammaherpesvirus 68.

Murine gammaherpesvirus 68 (MHV-68) is a naturally occurring rodent pathogen with significant homology to human pathogens Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus. T cells are essential for primary clearance of MHV-68 and survival of mice following intranasal infection. Previous reports have suggested that protein kinase C theta (PKCtheta) is essential for T-cell activation and cytokine production in vitro.

Chemokine expression during the development and resolution of a pulmonary leukocyte response to influenza A virus infection in mice.

Influenza A virus replicates in the respiratory epithelium and induces an inflammatory infiltrate comprised of mononuclear cells and neutrophils. To understand the development of the cell-mediated immune response to influenza and how leukocyte trafficking to sites of inflammation is regulated, we examined the chemokine expression pattern in lung tissue from A/PR/8/34-infected C57BL/6 mice using an RNase protection assay. Monocyte chemoattractant protein 1, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, MIP-3alpha, regulated on activation, normal T expressed and secreted (RANTES), MIP-2, and interferon-inducible protein 10 (IP-10) mRNA expression was up-regulated between days 5 and 15 after infection, consistent with a role for these chemokines in leukocyte recruitment to the lung.