Work

Inhibition of clonal expansion by Foxp3 expression as a mechanism of controlled T‐cell responses and autoimmune disease

Year: 2009

Type: article

Abstract: The essential role of the transcription factor Foxp3 in the development and function of Treg has been well documented. The role of Foxp3 in non-Treg, however, is not fully understood. Emerging evidence indicates that Foxp3 expression is not confined to CD4+CD25+ Treg. The present study shows that in Foxp3 transgenic (Foxp3-Tg) mice, in which the transgene is driven by the lck distal promoter, CD4+CD25- T cells that express the Foxp3 transgene do not upregulate the expression of CD25-, GITR, or CTLA-4, and do not have suppressive function; however, the Foxp3-Tg+CD4+CD25- T cells exhibit significantly reduced proliferative response to TCR engagement. Foxp3-Tg mice are resistant to collagen-induced arthritis via reduced cellular proliferation of activated T cells. These findings indicate that Foxp3 upregulation in activated non-Treg may be a mechanism to suppress immune responses by reduced clonal expansion of activated T cells.

Source: European Journal of Immunology

DOI: 10.1002/eji.200939404

Authors: Linjie Guo, Jun Tian, Ekaterina Marinova, Biao Zheng, Shuhua Han

Institution: Baylor College of Medicine

Language: English

Topic: T-cell and B-cell Immunology

Subfield: Immunology

Field: Immunology and Microbiology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: bronze

Funders: National Institutes of Health, National Institute of Allergy and Infectious Diseases