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- W4313305869 abstract "Abstract Mice deficient in the kinase, Drak2, are resistant to disease in mouse models of type 1 diabetes (T1D) and multiple sclerosis (MS) due to diminished survival of autoreactive T cells. Yet, Drak2-/- mice effectively eliminate infectious pathogens and retain the ability to combat tumors similar to wildtype mice. Thus, Drak2 is an ideal protein to target to treat autoimmune disorders without compromising immunity to infections or tumors. However, the molecular mechanisms and functions of Drak2 are unclear. It is important to discern how Drak2 contributes to T1D to further understand the etiology of this disease, as well as to validate Drak2 as a therapeutic target. We show here that the resistance to T1D in NOD.Drak2-/- mice was due to the absence of Drak2 in T cells rather than the pancreatic b-cells. Furthermore, the resistance to disease required regulatory T cells (Tregs). Interestingly, the development of thymic Tregs was increased in Drak2-/- mice due to augmented IL-2 signaling, which led to an increase in the proportion of Foxp3-expressing cells. These studies provide important insight into the etiology of T1D by showing that Drak2 contributes to autoimmune disease by reducing the proportion of Tregs through reduction of IL-2 signaling in T cells." @default.
- W4313305869 created "2023-01-06" @default.
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- W4313305869 date "2015-05-01" @default.
- W4313305869 modified "2023-09-27" @default.
- W4313305869 title "Drak2 contributes to type 1 diabetes by altering regulatory T cell development. (BA6P.128)" @default.
- W4313305869 doi "https://doi.org/10.4049/jimmunol.194.supp.114.9" @default.
- W4313305869 hasPublicationYear "2015" @default.
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