FOXP3 is essential for the development and function of regulatory CD4(+)CD25(hi) T (T(reg)) cells. However, recent evidence suggests that FOXP3 alone is not sufficient to completely explain the regulatory phenotype of these key players in autoimmunity and inflammation: after being activated, conventional human CD4(+) T cells transiently up-regulate FOXP3 without acquiring a regulatory function. Researchers have recently found that glycoprotein A repetitions predominant (GARP, or LRRC32) is a T(reg)-specific receptor that binds latent TGF-beta and dominantly controls FOXP3 and the regulatory phenotype via a positive feedback loop. This finding provides a missing link in our molecular understanding of FOXP3 in T(reg) cells. This viewpoint focuses on GARP as safeguard of FOXP3 and the regulatory phenotype.
CITATION STYLE
Probst-Kepper, M., Balling, R., & Buer, J. (2012). FOXP3: Required but Not Sufficient. The Role of GARP (LRRC32) as a Safeguard of the Regulatory Phenotype. Current Molecular Medicine, 10(6), 533–539. https://doi.org/10.2174/156652410792231349
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