{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T07:05:27Z","timestamp":1792047927700,"version":"4.4.0"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2020,8,1]],"date-time":"2020-08-01T00:00:00Z","timestamp":1596240000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>C-type lectin CLEC16A is located next to CIITA, the master transcription factor of HLA class II (HLA-II), at a susceptibility locus for several autoimmune diseases, including multiple sclerosis (MS). We previously found that CLEC16A promotes the biogenesis of HLA-II peptide-loading compartments (MIICs) in myeloid cells. Given the emerging role of B cells as APCs in these diseases, in this study, we addressed whether and how CLEC16A is involved in the BCR-dependent HLA-II pathway. CLEC16A was coexpressed with surface class II\u2013associated invariant chain peptides (CLIP) in human EBV-positive and not EBV-negative B cell lines. Stable knockdown of CLEC16A in EBV-positive Raji B cells resulted in an upregulation of surface HLA-DR and CD74 (invariant chain), whereas CLIP was slightly but significantly reduced. In addition, IgM-mediated Salmonella uptake was decreased, and MIICs were less clustered in CLEC16A-silenced Raji cells, implying that CLEC16A controls both HLA-DR\/CD74 and BCR\/Ag processing in MIICs. In primary B cells, CLEC16A was only induced under CLIP-stimulating conditions in vitro and was predominantly expressed in CLIPhigh naive populations. Finally, CLIP-loaded HLA-DR molecules were abnormally enriched, and coregulation with CLEC16A was abolished in blood B cells of patients who rapidly develop MS. These findings demonstrate that CLEC16A participates in the BCR-dependent HLA-II pathway in human B cells and that this regulation is impaired during MS disease onset. The abundance of CLIP already on naive B cells of MS patients may point to a chronically induced stage and a new mechanism underlying B cell\u2013mediated autoimmune diseases such as MS.<\/jats:p>","DOI":"10.4049\/jimmunol.1901409","type":"journal-article","created":{"date-parts":[[2020,7,8]],"date-time":"2020-07-08T20:25:21Z","timestamp":1594239921000},"page":"945-956","source":"Crossref","is-referenced-by-count":18,"title":["The Role of Autoimmunity-Related Gene <i>CLEC16A<\/i> in the B Cell Receptor\u2013Mediated HLA Class II Pathway"],"prefix":"10.1093","volume":"205","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2294-2774","authenticated-orcid":false,"given":"Liza","family":"Rijvers","sequence":"first","affiliation":[{"name":"Department of Immunology, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]},{"name":"MS Center ErasMS, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie-Jos\u00e9","family":"Melief","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]},{"name":"MS Center ErasMS, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamie","family":"van Langelaar","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]},{"name":"MS Center ErasMS, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roos M","family":"van der Vuurst de Vries","sequence":"additional","affiliation":[{"name":"MS Center ErasMS, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]},{"name":"Department of Neurology, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annet F","family":"Wierenga-Wolf","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]},{"name":"MS Center ErasMS, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven C","family":"Koetzier","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]},{"name":"MS Center ErasMS, Erasmus MC , 3015 CN Rotterdam ,","place":["the Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8794-6306","authenticated-orcid":false,"given":"John J","family":"Priatel","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, University of British Columbia , Vancouver, British Columbia V6T 1Z4 ,","place":["Canada"]},{"name":"BC Children\u2019s Hospital Research Institute , Vancouver, British Columbia V5Z 4H4 ,","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tineke","family":"Jorritsma","sequence":"additional","affiliation":[{"name":"Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam University Medical Center, University of Amsterdam , 1066 CX Amsterdam ,","place":["the Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S Marieke","family":"van Ham","sequence":"additional","affiliation":[{"name":"Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam University Medical Center, University of Amsterdam , 1066 CX Amsterdam ,","place":["the Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rogier Q","family":"Hintzen","sequence":"additional","affiliation":[{"name":"Department of Immunology, Erasmus MC , 3015 CN Rotterdam 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