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Self-Limitation of Th1-Mediated Inflammation by IFN-¹

Markus Feuerer^2,*, Katharina Eulenburg^*, Christoph Loddenkemper, Alf Hamann^* and Jochen Huehn^3,*

^* Experimentelle Rheumatologie, Charité Universitaetsmedizin Berlin, Campus Mitte, Berlin, Germany; and Institut fuer Pathologie, Charité Universitaetsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany

IFN- is an effector cytokine of cell-mediated immunity that plays an essential role in both innate and adaptive phases of an immune response. Interestingly, in several Th1-dependent autoimmune models, lack of IFN- is associated with an acceleration of disease. To distinguish the influence of IFN- on the polarization of naive precursors from the influence on effector cells, we used an adoptive transfer model of differentiated Ag-specific Th1 cells. In this study, IFN- displayed a dual function in a Th1-dependent immune reaction. In the early phase, IFN- accelerated the inflammation, whereas in the late phase it mediated the process of self-limitation. We demonstrated that IFN- limits the number of Th1 effector cells after Ag challenge. Studies using IFN-R^–/– mice as recipients showed that IFN- acts indirectly via host cells to regulate the pool size of Th1 cells. NO was a downstream effector molecule. Transfer experiments of Th1 cells into IFN-^–/– mice revealed that Th1 cells control both themselves and the corresponding inflammation by the release of IFN-. Thus, the proinflammatory cytokine IFN- can act as a negative feedback regulator to control Th1-mediated immune responses.

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