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- W4313351760 abstract "Abstract NF-κB-inducing kinase (NIK) is an essential upstream kinase in non-canonical, or alternative, NF-κB activation. TNF receptor family members such as BAFFR and LTβR depend on NIK for signaling, but little is known about the role of NIK downstream of TNF receptors in T cells. Here, we describe a T cell-intrinsic requirement for NIK in graft-versus-host disease (GvHD), wherein NIK-deficient alymphoplasia (aly) T cells transferred into MHC class II mismatched recipients fail to cause disease. We show that although NIK is not necessary for antigen receptor signaling, it is essential for costimulation through the TNF receptor family member OX40 (CD134). Notably, OX40 deficient T cells also fail to elicit GvHD. To assess whether NIK overexpression could recapitulate chronic OX40 activation, we conditionally overexpressed NIK in T cells in vivo using a Cre-inducible transgene. Mice with modest NIK overexpression limited to T cells suffered rapid fatal autoimmunity characterized by hyperactive effector T cells and poorly suppressive Foxp3+ regulatory T cells. Together, these data reveal a critical T cell-intrinsic role for NIK during immune responses, and suggest that tight regulation of the non-canonical NF-κB pathway is crucial to avoid autoimmunity." @default.
- W4313351760 created "2023-01-06" @default.
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- W4313351760 date "2011-04-01" @default.
- W4313351760 modified "2023-10-01" @default.
- W4313351760 title "NF-κB-inducing kinase plays an essential T cell intrinsic role in graft-versus-host disease and OX40-mediated costimulation, and its overexpression causes lethal autoimmunity (63.3)" @default.
- W4313351760 doi "https://doi.org/10.4049/jimmunol.186.supp.63.3" @default.
- W4313351760 hasPublicationYear "2011" @default.
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