English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

The transcription factor RORγt regulates differentiation of the T H 17 subset of helper T cells, thymic T cell development and lymph-node genesis. Although elimination of RORγt prevents T H 17 cell-mediated experimental autoimmune encephalomyelitis (EAE), it also disrupts thymocyte development, which could lead to lethal thymic lymphoma. Here we identified a two-amino-acid substitution in RORγt (RORγt M ) that 'preferentially' disrupted T H 17 differentiation but not thymocyte development. Mice expressing RORγt M were resistant to EAE associated with defective T H 17 differentiation but maintained normal thymocyte development and normal lymph-node genesis, except for Peyer's patches. RORγt M showed less ubiquitination at Lys69 that was selectively required for T H 17 differentiation but not T cell development. This study will inform the development of treatments that selectively target T H 17 cell-mediated autoimmunity but do not affect thymocyte development or induce lymphoma.

A two-amino-acid substitution in the transcription factor RORγt disrupts its function in TH17 differentiation but not in thymocyte development