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Reißig, S.* ; Tang, Y.* ; Nikolaev, A.* ; Gerlach, K.* ; Wolf, C. ; Davari, K. ; Gallus, C. ; Masri, J.* ; Mufazalov, I.A.* ; Neurath, M.F.* ; Wunderlich, F.T.* ; Schattenberg, J.M.* ; Galle, P.R.* ; Weigmann, B.* ; Waisman, A.* ; Glasmacher, E. ; Hövelmeyer, N.*

Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis.

Nat. Commun. 8:15069 (2017)

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Bcl-3 is an atypical NF-κB family member that regulates NF-κB-dependent gene expression in effector T cells, but a cell-intrinsic function in regulatory T (Treg) cells and colitis is not clear. Here we show that Bcl-3 expression levels in colonic T cells correlate with disease manifestation in patients with inflammatory bowel disease. Mice with T-cell-specific overexpression of Bcl-3 develop severe colitis that can be attributed to defective Treg cell development and function, leading to the infiltration of immune cells such as pro-inflammatory γδT cells, but not αβ T cells. In Treg cells, Bcl-3 associates directly with NF-κB p50 to inhibit DNA binding of p50/p50 and p50/p65 NF-κB dimers, thereby regulating NF-κB-mediated gene expression. This study thus reveals intrinsic functions of Bcl-3 in Treg cells, identifies Bcl-3 as a potential prognostic marker for colitis and illustrates the mechanism by which Bcl-3 regulates NF-κB activity in Tregs to prevent colitis.

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