Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Pollard, K.M. et al.

K. Michael Pollard, Per Hultman, Christopher B. Toomey, David M. Cauvi, Hal M. Hoffman, John C. Hamel, Dwight H. Kono, Per Hultman, Christopher B. Toomey, David M. Cauvi, Hal M. Hoffman, John C. Hamel, Dwight H. Kono,

Definition of IFN-γ-related pathways critical for chemically-induced systemic autoimmunity.

IFN-γ is essential for idiopathic and murine mercury-induced systemic autoimmunity (mHgIA), and heterozygous IFN-γ(+/-) mice also exhibit reduced disease. This suggests that blocking specific IFN-γ-related pathways that may only partially inhibit IFN-γ production or function will also suppress autoimmunity. To test this hypothesis, mice deficient in genes regulating IFN-γ expression (Casp1, Nlrp3, Il12a, Il12b, Stat4) or function (Ifngr1, Irf1) were examined for mHgIA susceptibility. Absence of either Ifngr1 or Irf1 resulted in a striking reduction of disease, while deficiency of genes promoting IFN-γ expression had modest to no effect. Furthermore, both Irf1- and Ifng-deficiency only modestly reduced the expansion of CD44(hi) and CD44(hi)CD55(lo) CD4(+) T cells, indicating that they are not absolutely required for T cell activation. Thus, there is substantial redundancy in genes that regulate IFN-γ expression in contrast to those that mediate later signaling events. These findings have implications for the therapeutic targeting of IFN-γ pathways in systemic autoimmunity.[1]

References

Definition of IFN-γ-related pathways critical for chemically-induced systemic autoimmunity. Pollard, K.M., Hultman, P., Toomey, C.B., Cauvi, D.M., Hoffman, H.M., Hamel, J.C., Kono, D.H. J. Autoimmun. (2012) [Pubmed]

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