| First Author | Ortega-Francisco S | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 494 |
| Issue | 1-2 | Pages | 82-87 |
| PubMed ID | 29050936 | Mgi Jnum | J:251047 |
| Mgi Id | MGI:6102968 | Doi | 10.1016/j.bbrc.2017.10.081 |
| Citation | Ortega-Francisco S, et al. (2017) TbetaRIII is induced by TCR signaling and downregulated in FoxP3(+) regulatory T cells. Biochem Biophys Res Commun 494(1-2):82-87 |
| abstractText | TGF-beta type III receptor (TbetaRIII) is a co-receptor for TGFbeta family members required for high-affinity binding of these ligands to their receptors, potentiating their cellular functions. TGF-betas, Bone Morphogenetic Proteins (BMP2/4) and Inhibins/Activins regulate different checkpoints during T cell differentiation. We have previously reported that TbetaRIII modulates T cell development by protecting developing thymocytes from apoptosis, however the role of this co-receptor in peripheral lymphocytes still remains elusive. Here we describe a detailed characterization of TbetaRIII expression in murine and human lymphocyte subpopulations demonstrating that this co-receptor is significantly expressed in T but not B lymphocytes and among them, preferentially expressed on naive and central memory T cells. TbetaRIII was upregulated after TCR stimulation, in parallel to other early activation markers. In contrast, natural and induced Tregs downregulated TbetaRIII in association with FoxP3 upregulation. Finally, anti-TbetaRIII blocking experiments demonstrated that TbetaRIII promotes TGFbeta-dependent iTreg conversion in vitro, and suggest that this co-receptor may be involved in modulating peripheral T cell tolerance and could be considered as a potential target to boost T cell immune responses. |
