CD9 regulates MHC-II trafficking in Monocyte-derived Dendritic Cells. Rocha-Perugini, V., Martínez Del Hoyo, G., González-Granado, J. M., Ramírez-Huesca, M., Zorita, V., Rubinstein, E., Boucheix, C., & Sánchez-Madrid, F. Molecular and Cellular Biology, May, 2017. doi abstract bibtex Antigen presentation by dendritic cells (DCs) stimulates naïve CD4(+) T cells, triggering T cell activation and the adaptive arm of the immune response. Newly synthesized major histocompatibility complex class II molecules (MHC-II) accumulate at MHC-II-enriched endosomal compartments, and are transported to the plasma membrane of DCs after binding to antigenic peptides to enable antigen presentation. In DCs, MHC-II molecules are included in tetraspanin-enriched microdomains (TEMs). However, the role of tetraspanin CD9 in these processes remains largely undefined. Here, we show that CD9 regulates the T-cell stimulatory capacity of GM-CSF-dependent bone-marrow derived DCs (BMDCs), without affecting antigen-presentation by Flt3L-dependent BMDCs. CD9 knock-out (KO) GM-CSF-dependent BMDCs, which resemble monocyte-derived DCs (MoDCs) induce lower T cell activation than wild-type DCs, and this effect is related to a reduction in MHC-II surface expression in CD9-deficient MoDCs. Importantly, MHC-II targeting to the plasma membrane is largely impaired in immature MoDCs from CD9 KO, in which MHC-II remains arrested in acidic intracellular compartments enriched in LAMP-1, and MHC-II internalization is also blocked. Moreover, CD9 participates in MHC-II trafficking in mature MoDCs, regulating its endocytosis and recycling. Our results demonstrate that the tetraspanin CD9 specifically regulates antigenic presentation in MoDCs through the regulation of MHC-II intracellular trafficking.
@article{rocha-perugini_cd9_2017,
title = {{CD9} regulates {MHC}-{II} trafficking in {Monocyte}-derived {Dendritic} {Cells}},
issn = {1098-5549},
doi = {10.1128/MCB.00202-17},
abstract = {Antigen presentation by dendritic cells (DCs) stimulates naïve CD4(+) T cells, triggering T cell activation and the adaptive arm of the immune response. Newly synthesized major histocompatibility complex class II molecules (MHC-II) accumulate at MHC-II-enriched endosomal compartments, and are transported to the plasma membrane of DCs after binding to antigenic peptides to enable antigen presentation. In DCs, MHC-II molecules are included in tetraspanin-enriched microdomains (TEMs). However, the role of tetraspanin CD9 in these processes remains largely undefined. Here, we show that CD9 regulates the T-cell stimulatory capacity of GM-CSF-dependent bone-marrow derived DCs (BMDCs), without affecting antigen-presentation by Flt3L-dependent BMDCs. CD9 knock-out (KO) GM-CSF-dependent BMDCs, which resemble monocyte-derived DCs (MoDCs) induce lower T cell activation than wild-type DCs, and this effect is related to a reduction in MHC-II surface expression in CD9-deficient MoDCs. Importantly, MHC-II targeting to the plasma membrane is largely impaired in immature MoDCs from CD9 KO, in which MHC-II remains arrested in acidic intracellular compartments enriched in LAMP-1, and MHC-II internalization is also blocked. Moreover, CD9 participates in MHC-II trafficking in mature MoDCs, regulating its endocytosis and recycling. Our results demonstrate that the tetraspanin CD9 specifically regulates antigenic presentation in MoDCs through the regulation of MHC-II intracellular trafficking.},
language = {eng},
journal = {Molecular and Cellular Biology},
author = {Rocha-Perugini, Vera and Martínez Del Hoyo, Gloria and González-Granado, José Maria and Ramírez-Huesca, Marta and Zorita, Virginia and Rubinstein, Eric and Boucheix, Claude and Sánchez-Madrid, Francisco},
month = may,
year = {2017},
pmid = {28533221},
}
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In DCs, MHC-II molecules are included in tetraspanin-enriched microdomains (TEMs). However, the role of tetraspanin CD9 in these processes remains largely undefined. Here, we show that CD9 regulates the T-cell stimulatory capacity of GM-CSF-dependent bone-marrow derived DCs (BMDCs), without affecting antigen-presentation by Flt3L-dependent BMDCs. CD9 knock-out (KO) GM-CSF-dependent BMDCs, which resemble monocyte-derived DCs (MoDCs) induce lower T cell activation than wild-type DCs, and this effect is related to a reduction in MHC-II surface expression in CD9-deficient MoDCs. Importantly, MHC-II targeting to the plasma membrane is largely impaired in immature MoDCs from CD9 KO, in which MHC-II remains arrested in acidic intracellular compartments enriched in LAMP-1, and MHC-II internalization is also blocked. Moreover, CD9 participates in MHC-II trafficking in mature MoDCs, regulating its endocytosis and recycling. 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