期刊
BLOOD
卷 113, 期 6, 页码 1268-1277出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2008-07-166553
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资金
- Academy of Finland (Helsinki, Finland)
- Sigrid Juselius Foundation (Helsinki, Finland)
- Department of Biotechnology, Government of India (New Delhi, India)
- National Technology Agency (TEKES
- Helsinki, Finland)
- Turku University Hospital Fund (Turku, Finland)
- Varino and Laina Kivi Foundation (Huittinen, Finland)
- Pulmonary Association Heli (Helsinki, Finland)
- Ida Montin Foundation (Helsinki, Finland)
- Finnish Cultural Foundation (Helsinki, Finland)
The identification of novel factors regulating human T helper (Th)-cell differentiation into functionally distinct Th1 and Th2 subsets is important for understanding the mechanisms behind human autoimmune and allergic diseases. We have identified a protein of relevant evolutionary and lymphoid interest (PRELI), a novel protein that induces oxidative stress and a mitochondrial apoptosis pathway in human primary Th cells. We also demonstrated that PRELI inhibits Th2-cell development and down-regulates signal transducer and activator of transcription 6 (STAT6), a key transcription factor driving Th2 differentiation. Our data suggest that calpain, an oxidative stress-induced cysteine protease, is involved in the PRELI-induced down-regulation of STAT6. Moreover, we observed that a strong T-cell receptor (TCR) stimulus induces expression of PRELI and inhibits Th2 development. Our results suggest that PRELI is involved in a mechanism wherein the strength of the TCR stimulus influences the polarization of Th cells. This study identifies PRELI as a novel factor influencing the human primary Th-cell death and differentiation. (Blood. 2009; 113: 1268-1277)
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