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In vivo generation of pathogen-specific Th1 cells in the absence of the IFN-gamma receptor
Journal article   Peer reviewed

In vivo generation of pathogen-specific Th1 cells in the absence of the IFN-gamma receptor

Jodie S Haring, Vladimir P Badovinac, Matthew R Olson, Steven M Varga and John T Harty
The Journal of immunology (1950), Vol.175(5), pp.3117-3122
09/01/2005
DOI: 10.4049/jimmunol.175.5.3117
PMID: 16116201

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Abstract

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-gammaR 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-gamma 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-gamma, Ag-specific CD4 T cells were generated in response to both these infections. In addition, IFN-gamma-producing (Th1) Ag-specific CD4 T cells were generated in mice lacking the ligand-binding chain of the IFN-gammaR (IFN-gammaR1-/-) or the signaling chain (IFN-gammaR2-/-). 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-gamma signaling, indicating that the cells were committed Th1 cells. Thus, both chains of the IFN-gammaR are dispensable for the generation of Th1 Ag-specific CD4 T cells after infection in vivo.
 Th1 Cells - physiology Animals Hemolysin Proteins Bacterial Toxins - immunology Mice, Inbred C57BL Peptide Fragments - immunology Interferon-gamma - physiology Receptors, Interferon - physiology Mice Heat-Shock Proteins - immunology

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