Cleavage of roquin and regnase-1 by the paracaspase MALT1 releases their cooperatively repressed targets to promote [T.sub.H]17 differentiation
Humoral autoimmunity paralleled by the accumulation of follicular helper T cells (TFH cells) is linked to mutation of the gene encoding the RNA-binding protein roquin-1. Here we found that T cells lacking roquin caused pathology in the lung and accumulated as cells of the [T.sub.H]17 subset of helpe...
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| Veröffentlicht in: | Nature immunology 2014-11, Vol.15 (11), p.1079 |
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| creator | Jeltsch, Katharina M Hu, Desheng Brenner, Sven Zoller, Jessica Heinz, Gitta A Nagel, Daniel Vogel, Katharina U Rehage, Nina Warth, Sebastian C Edelmann, Stephanie L Gloury, Renee Martin, Nina Lohs, Claudia Lech, Maciej Stehklein, Jenny E Geerlof, Arie Kremmer, Elisabeth Weber, Achim Anders, Hans-Joachim Schmitz, Ingo Schmidt-Supprian, Marc Fu, Mingui Holtmann, Helmut Krappmann, Daniel Ruland, Jurgen Kallies, Axel Heikenwalder, Mathias Heissmeyer, Vigo |
| description | Humoral autoimmunity paralleled by the accumulation of follicular helper T cells (TFH cells) is linked to mutation of the gene encoding the RNA-binding protein roquin-1. Here we found that T cells lacking roquin caused pathology in the lung and accumulated as cells of the [T.sub.H]17 subset of helper T cells in the lungs. Roquin inhibited [T.sub.H]17 cell differentiation and acted together with the endoribonuclease regnase-1 to repress target mRNA encoding the [T.sub.H]17 cell-promoting factors IL-6, ICOS, c-Rel, IRF4, IkBNS and Ik Be This cooperation required binding of RNA by roquin and the nuclease activity of regnase-1. Upon recognition of antigen by the T cell antigen receptor (TCR), roquin and regnase-1 proteins were cleaved by the paracaspase MALT1. Thus, this pathway acts as a 'rheostat' by translating TCR signal strength via graded inactivation of post-transcriptional repressors and differential derepression of targets to enhance [T.sub.H]17 differentiation. |
| doi_str_mv | 10.1038/ni.3008 |
| format | Article |
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Here we found that T cells lacking roquin caused pathology in the lung and accumulated as cells of the [T.sub.H]17 subset of helper T cells in the lungs. Roquin inhibited [T.sub.H]17 cell differentiation and acted together with the endoribonuclease regnase-1 to repress target mRNA encoding the [T.sub.H]17 cell-promoting factors IL-6, ICOS, c-Rel, IRF4, IkBNS and Ik Be This cooperation required binding of RNA by roquin and the nuclease activity of regnase-1. Upon recognition of antigen by the T cell antigen receptor (TCR), roquin and regnase-1 proteins were cleaved by the paracaspase MALT1. Thus, this pathway acts as a 'rheostat' by translating TCR signal strength via graded inactivation of post-transcriptional repressors and differential derepression of targets to enhance [T.sub.H]17 differentiation.</abstract><pub>Nature Publishing Group</pub><doi>10.1038/ni.3008</doi><tpages>13</tpages></addata></record> |
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| subjects | Binding proteins Cell differentiation Genetic aspects Properties T cells |
| title | Cleavage of roquin and regnase-1 by the paracaspase MALT1 releases their cooperatively repressed targets to promote [T.sub.H]17 differentiation |
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