FOXP3: required but not sufficient. the role of GARP (LRRC32) as a safeguard of the regulatory phenotype

Current Molecular Medicine
Michael Probst-KepperJan Buer

Abstract

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.

Citations

Jun 7, 2012·Transfusion Medicine and Hemotherapy : Offizielles Organ Der Deutschen Gesellschaft Fur̈ Transfusionsmedizin Und Immunham̈atologie·Jan KehrmannMichael Probst-Kepper
Feb 9, 2010·Biology Direct·Michael Probst-Kepper, Jan Buer
Feb 6, 2013·PloS One·Ellen L GoodeKeith L Knutson
Aug 18, 2012·Wiley Interdisciplinary Reviews. Systems Biology and Medicine·Feng He, Rudi Balling

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