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Osteopontin Is Not Required for the Development of Th1 Responses and Viral Immunity¹

Brian Abel^*, Stefan Freigang, Martin F. Bachmann, Ursula Boschert and Manfred Kopf^2,*

^* Molecular Biomedicine, Swiss Federal Institute of Technology, and Cytos Biotechnology AG, Zurich-Schlieren, Switzerland; Institute for Experimental Immunology, Zurich, Switzerland; and Department of Immunology, Serono Pharmaceutical Research Institute, Geneva, Switzerland

Osteopontin (OPN) has been defined as a key cytokine promoting the release of IL-12 and hence inducing the development of protective cell-mediated immunity to viruses and intracellular pathogens. To further characterize the role of OPN in antiviral immunity, OPN-deficient (OPN^–/–) mice were analyzed after infection with influenza virus and vaccinia virus. Surprisingly, we found that viral clearance, lung inflammation, and recruitment of effector T cells to the lung were unaffected in OPN^–/– mice after influenza infection. Furthermore, effector status of T cells was normal as demonstrated by normal IFN- production and CTL lytic activity. Moreover, activation and Th1 differentiation of naive TCR transgenic CD4⁺ T cells by dendritic cells and cognate Ag was normal in the absence of OPN in vitro. Contrary to a previous report, we found that OPN^–/– mice mounted a normal immune response to Listeria monocytogenes. In conclusion, OPN is dispensable for antiviral immune responses against influenza virus and vaccinia virus.

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