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CUTTING EDGE |
* The Edward Jenner Institute for Vaccine Research, Compton, Newbury, Berkshire, United Kingdom; and
Department of Immunology, Paul Ehrlich Institute, Langen, Germany
Type I IFN (IFN-
) is induced rapidly by infection and plays a key role in innate antiviral defense. IFN- also exerts stimulatory effects on the adaptive immune system and has been shown to enhance Ab and T cell responses. We have investigated the importance of B and T cells as direct targets of IFN- during IFN--mediated augmentation of the Ab response against a soluble protein Ag. Strikingly, the ability of IFN- to stimulate the Ab response and induce isotype switching was markedly reduced in mice in which B cells were selectively deficient for the IFN-R. Moreover, IFN--mediated enhancement of the Ab response was also greatly impaired in mice in which T cells were selectively IFN-R-deficient. These results indicate that IFN-R signaling in both B and T cells plays an important role in the stimulation of Ab responses by IFN-.
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