| http://purl.uniprot.org/citations/15652415 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15652415 | http://www.w3.org/2000/01/rdf-schema#comment | "Peripheral antigen presenting cells (APCs) contribute to the maintenance of immune tolerance and are considered to play a critical role in promoting the (re)activation of autoreactive T cells in multiple sclerosis (MS). Interferon-beta (IFN-beta) is the principle immune-modulatory agent used in the treatment of MS, but its mechanism of action remains elusive. HLA-G is a non-classical MHC molecule (MHC class Ib) attributed chiefly immune-regulatory functions. We here investigated the role of monocyte-derived HLA-G in the immune-regulatory processes of MS and its implications for current immune-modulatory therapies. Monocytes constitutively express cell surface HLA-G1 and soluble HLA-G5. Comparison of monocytic HLA-G expression between patients with relapsing-remitting MS (n=17) and healthy donors (n=20) revealed significantly lower levels of HLA-G1 protein in MS patients. However, both groups showed a significant upregulation of HLA-G in response to IFN-beta in vitro. Serial measurements of HLA-G mRNA levels in MS patients before and during IFN-beta therapy corroborated the relevance of these results in vivo: 1 month after initiation of IFN-beta1b therapy (n=9), HLA-G1 and HLA-G5 were significantly increased compared to baseline levels and remained elevated during treatment for 6 months (n=3). Importantly, functional experiments demonstrated that monocyte-derived HLA-G inhibits both Th1 (IFN-gamma, IL-2) and Th2 (IL-10) cytokine production by antigen-stimulated autologous CD4 T cells. Soluble HLA-G added to antigen-specific T cell lines (TCLs) has similar effects on the release of cytokines and reduces T cell proliferation. Although both IFN-beta and IFN-gamma strongly enhance HLA-G1 and HLA-G5 expression by monocytes in vitro, IFN-beta leads to a stronger relative upregulation of HLA-G compared to classical MHC class I molecules than stimulation with IFN-gamma. Taken together, monocyte-derived HLA-G mediates the inhibition of autologous CD4 T cell activation and might be involved in immune-regulatory pathways in the pathogenesis of MS. We conclude that some desirable immune-modulatory effects of INF-beta might be accomplished via the upregulation of the immune-tolerogenic molecule HLA-G."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.jneuroim.2004.09.016"xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/author | "Hartung H.P."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/author | "Weller M."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/author | "Wiendl H."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/author | "Dichgans J."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/author | "Schreiner B."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/author | "Neuhaus O."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/author | "Kieseier B.C."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/author | "Mitsdoerffer M."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/name | "J Neuroimmunol"xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/pages | "155-164"xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/title | "Monocyte-derived HLA-G acts as a strong inhibitor of autologous CD4 T cell activation and is upregulated by interferon-beta in vitro and in vivo: rationale for the therapy of multiple sclerosis."xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://purl.uniprot.org/core/volume | "159"xsd:string |
| http://purl.uniprot.org/citations/15652415 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15652415 |
| http://purl.uniprot.org/citations/15652415 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15652415 |
| http://purl.uniprot.org/uniprot/#_A0A0H4M9X9-mappedCitation-15652415 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15652415 |
| http://purl.uniprot.org/uniprot/#_A0A0H4M9Y0-mappedCitation-15652415 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15652415 |
| http://purl.uniprot.org/uniprot/#_A0A0H4M9Y1-mappedCitation-15652415 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15652415 |
| http://purl.uniprot.org/uniprot/#_A0A0H4M9Y2-mappedCitation-15652415 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15652415 |
| http://purl.uniprot.org/uniprot/#_A0A0H4M9Y3-mappedCitation-15652415 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15652415 |
| http://purl.uniprot.org/uniprot/#_A0A0H4M9Y6-mappedCitation-15652415 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15652415 |
| http://purl.uniprot.org/uniprot/#_A0A0H4M9Z1-mappedCitation-15652415 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15652415 |