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In Vivo Generation of Pathogen-Specific Th1 Cells in the Absence of the IFN- Receptor¹

Jodie S. Haring^*, Vladimir P. Badovinac^*, Matthew R. Olson^*, Steven M. Varga^* and John T. Harty^2,*,

^* Department of Microbiology and Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242

The precise mechanisms that govern the commitment of CD4 T cells to become Th1 or Th2 cells in vivo are incompletely understood. Recent experiments demonstrate colocalization of the IFN-R chains with the TCR during activation of naive CD4 T cells, suggesting that association of these molecules may be involved in determining lineage commitment. To test the role of IFN- and its receptor in the generation of Th1 Ag-specific CD4 T cells, we analyzed mice after infection with Listeria monocytogenes or lymphocytic choriomeningitis virus. In the absence of IFN-, Ag-specific CD4 T cells were generated in response to both these infections. In addition, IFN--producing (Th1) Ag-specific CD4 T cells were generated in mice lacking the ligand-binding chain of the IFN-R (IFN-R1^–/–) or the signaling chain (IFN-R2^–/–). There was no increase in the number of IL-4-producing Ag-specific CD4 T cells, nor was there a decrease in the expression of T-bet in the absence of functional IFN- signaling, indicating that the cells were committed Th1 cells. Thus, both chains of the IFN-R are dispensable for the generation of Th1 Ag-specific CD4 T cells after infection in vivo.

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