Cutting Edge: Requirement of MARCH-I-Mediated MHC II Ubiquitination for the Maintenance of Conventional Dendritic Cells
MARCH-I (membrane-associated RING-CH I) has been suggested as a physiological E3 ubiquitin ligase for both MHC class II (MHC II) and B7-2. In this study, we show that MARCH-I-mediated MHC II ubiquitination is necessary for the maintenance of conventional dendritic cell (cDC) functions in the steady...
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| Veröffentlicht in: | The Journal of immunology (1950) 2009-12, Vol.183 (11), p.6893-6897 |
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| container_title | The Journal of immunology (1950) |
| container_volume | 183 |
| creator | Ohmura-Hoshino, Mari Matsuki, Yohei Mito-Yoshida, Mari Goto, Eiji Aoki-Kawasumi, Masami Nakayama, Manabu Ohara, Osamu Ishido, Satoshi |
| description | MARCH-I (membrane-associated RING-CH I) has been suggested as a physiological E3 ubiquitin ligase for both MHC class II (MHC II) and B7-2. In this study, we show that MARCH-I-mediated MHC II ubiquitination is necessary for the maintenance of conventional dendritic cell (cDC) functions in the steady state. MARCH-I-deficient cDCs accumulated MHC II and B7-2 and exhibited low Ag-presenting ability for exogenous Ags and low cytokine-producing ability upon stimulation in vivo. Importantly, MHC II, but not B7-2, was required for impaired cDC function induced by loss of MARCH-I in vivo. Moreover, MHC II knockin mice whose MHC II was not ubiquitinated showed dysfunction of cDC similar to that of MARCH-I knockout mice. These results suggest that the accumulation of MHC II resulting from loss of ubiquitination caused cDC abnormality; therefore, MARCH-I may function as a housekeeper of cDC in the steady state. |
| doi_str_mv | 10.4049/jimmunol.0902178 |
| format | Article |
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In this study, we show that MARCH-I-mediated MHC II ubiquitination is necessary for the maintenance of conventional dendritic cell (cDC) functions in the steady state. MARCH-I-deficient cDCs accumulated MHC II and B7-2 and exhibited low Ag-presenting ability for exogenous Ags and low cytokine-producing ability upon stimulation in vivo. Importantly, MHC II, but not B7-2, was required for impaired cDC function induced by loss of MARCH-I in vivo. Moreover, MHC II knockin mice whose MHC II was not ubiquitinated showed dysfunction of cDC similar to that of MARCH-I knockout mice. These results suggest that the accumulation of MHC II resulting from loss of ubiquitination caused cDC abnormality; therefore, MARCH-I may function as a housekeeper of cDC in the steady state.</description><subject>Animals</subject><subject>Antigen Presentation - immunology</subject><subject>B7-2 Antigen - biosynthesis</subject><subject>B7-2 Antigen - immunology</subject><subject>CD4 Antigens - biosynthesis</subject><subject>CD4 Antigens - immunology</subject><subject>CD8 Antigens - biosynthesis</subject><subject>CD8 Antigens - immunology</subject><subject>Dendritic Cells - immunology</subject><subject>Dendritic Cells - metabolism</subject><subject>Flow Cytometry</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation - immunology</subject><subject>Gene Knock-In Techniques</subject><subject>Genes, MHC Class II</subject><subject>Histocompatibility Antigens Class II - genetics</subject><subject>Histocompatibility Antigens Class II - immunology</subject><subject>Histocompatibility Antigens Class II - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Ubiquitin-Protein Ligases - genetics</subject><subject>Ubiquitin-Protein Ligases - immunology</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><subject>Ubiquitination - physiology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtP3DAURi1UVAbaPavKu3YTem0nfnSHUigjMUJCZW15kpsZo8SB2CHqv6_RTNWVJeucz9Yh5JLBVQml-f7sh2EOY38FBjhT-oSsWFVBISXID2QFwHnBlFRn5DzGZwCQwMuP5IwZk681X5GlnlPyYUdv2h3-oI_4OvsJBwyJjh3dXD_Wd8W62GDrXcKWbu5qul7Tp63PXPZc8mOg3TjRtEe6cT4kDC40-G7XY3jLQ5lwPf2JoZ2y0tAa-z5-Iqed6yN-Pp4X5On25nd-7P7h17q-vi-aUphUqM5pqVSFreCGN2brlBKmEq3WjLNGcCi50VsuddMpZlwlFIKrZNsJVKArcUG-HnZfpvF1xpjs4GOTf-ACjnO0SpSsVJWCTMKBbKYxxgk7-zL5wU1_LAP7Xtv-q22PtbPy5Tg-bwds_wvHvBn4dgD2frdfclgbB9f3GWd2WRamhWXMSm2E-Au0zomp</recordid><startdate>20091201</startdate><enddate>20091201</enddate><creator>Ohmura-Hoshino, Mari</creator><creator>Matsuki, Yohei</creator><creator>Mito-Yoshida, Mari</creator><creator>Goto, Eiji</creator><creator>Aoki-Kawasumi, Masami</creator><creator>Nakayama, Manabu</creator><creator>Ohara, Osamu</creator><creator>Ishido, Satoshi</creator><general>Am Assoc Immnol</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20091201</creationdate><title>Cutting Edge: Requirement of MARCH-I-Mediated MHC II Ubiquitination for the Maintenance of Conventional Dendritic Cells</title><author>Ohmura-Hoshino, Mari ; 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In this study, we show that MARCH-I-mediated MHC II ubiquitination is necessary for the maintenance of conventional dendritic cell (cDC) functions in the steady state. MARCH-I-deficient cDCs accumulated MHC II and B7-2 and exhibited low Ag-presenting ability for exogenous Ags and low cytokine-producing ability upon stimulation in vivo. Importantly, MHC II, but not B7-2, was required for impaired cDC function induced by loss of MARCH-I in vivo. Moreover, MHC II knockin mice whose MHC II was not ubiquitinated showed dysfunction of cDC similar to that of MARCH-I knockout mice. These results suggest that the accumulation of MHC II resulting from loss of ubiquitination caused cDC abnormality; therefore, MARCH-I may function as a housekeeper of cDC in the steady state.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>19917682</pmid><doi>10.4049/jimmunol.0902178</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antigen Presentation - immunology B7-2 Antigen - biosynthesis B7-2 Antigen - immunology CD4 Antigens - biosynthesis CD4 Antigens - immunology CD8 Antigens - biosynthesis CD8 Antigens - immunology Dendritic Cells - immunology Dendritic Cells - metabolism Flow Cytometry Gene Expression Gene Expression Regulation - immunology Gene Knock-In Techniques Genes, MHC Class II Histocompatibility Antigens Class II - genetics Histocompatibility Antigens Class II - immunology Histocompatibility Antigens Class II - metabolism Mice Mice, Inbred C57BL Mice, Knockout Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - immunology Ubiquitin-Protein Ligases - metabolism Ubiquitination - physiology |
| title | Cutting Edge: Requirement of MARCH-I-Mediated MHC II Ubiquitination for the Maintenance of Conventional Dendritic Cells |
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