TRIM28 prevents autoinflammatory T cell development in vivo

Shunsuke Chikuma, Naomasa Suita, Il Mi Okazaki, Shiro Shibayama, Tasuku Honjo

Research output: Contribution to journalArticlepeer-review

80 Citations (Scopus)


TRIM28 is a component of heterochromatin complexes whose function in the immune system is unknown. By studying mice with conditional T cell-specific deletion of TRIM28 (CKO mice), we found that TRIM28 was phosphorylated after stimulation via the T cell antigen receptor (TCR) and was involved in the global regulation of CD4+ T cells. The CKO mice had a spontaneous autoimmune phenotype that was due in part to early lymphopenia associated with a defect in the production of interleukin 2 (IL-2) as well as incomplete cell-cycle progression of their T cells. In addition, CKO T cells showed derepression of the cytokine TGF-β3, which resulted in an altered cytokine balance; this caused the accumulation of autoreactive cells of the T H17 subset of helper T cells and of Foxp3+ T cells. Notably, CKO Foxp3+ T cells were unable to prevent the autoimmune phenotype in vivo. Our results show critical roles for TRIM28 in both T cell activation and T cell tolerance.

Original languageEnglish
Pages (from-to)596-603
Number of pages8
JournalNature Immunology
Issue number6
Publication statusPublished - 2012 Jun
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


Dive into the research topics of 'TRIM28 prevents autoinflammatory T cell development in vivo'. Together they form a unique fingerprint.

Cite this