The paradox of high availability and low recognition of soluble HLA-G by LILRB1 receptor in rheumatoid arthritis patients
dc.contributor.author | Veit, Tiago Degani | pt_BR |
dc.contributor.author | Chies, Jose Artur Bogo | pt_BR |
dc.contributor.author | Switala, Magdalena | pt_BR |
dc.contributor.author | Wagner, Bettina | pt_BR |
dc.contributor.author | Horn, Peter A. | pt_BR |
dc.contributor.author | Busatto, Mauricio | pt_BR |
dc.contributor.author | Brenol, Claiton Viegas | pt_BR |
dc.contributor.author | Brenol, João Carlos Tavares | pt_BR |
dc.contributor.author | Xavier, Ricardo Machado | pt_BR |
dc.contributor.author | Rebmann, Vera | pt_BR |
dc.date.accessioned | 2018-04-26T02:33:07Z | pt_BR |
dc.date.issued | 2015 | pt_BR |
dc.identifier.issn | 1932-6203 | pt_BR |
dc.identifier.uri | http://hdl.handle.net/10183/175047 | pt_BR |
dc.description.abstract | HLA-G is a regulatory molecule involved in immunologic tolerance. Growing evidence indicates that HLA-G plays a role in the regulation of inflammatory processes and autoimmune diseases. This study aimed at a systematic evaluation of soluble HLA-G (sHLA-G) in plasma of rheumatoid arthritis (RA) patients with long-lasting chronic inflammation. RA patients (n=68) and healthy controls (n=26) had their plasmatic sHLA-G measured by ELISA whereas the binding capability of sHLA-G to its cognate LILRB1 receptor was measured by a Luminex-based assay. All subjects were PCR-genotyped for HLA-G 14bp polymorphism (rs66554220). Significantly higher sHLA-G levels were observed in patients (p<0.001), however no significant differences were observed in LILRB1 binding capacity between RA patients and controls. Remarkably, the proportion of patients presenting specific binding of sHLA-G to LILRB1 was significantly decreased as compared to controls (56% vs. 81%, p=0.027). Patients without rheumatoid factor (RF-) were significantly overrepresented in the group of patients positive for LILRB1 binding as compared to patients without LILRB1 binding (31% vs 10%, p=0.033). Furthermore, methotrexate treated patients (n=58) revealed significantly lower LILRB1 binding to sHLA-G molecules than non-treated patients (medians: 12.2 vs. 67.7 units/ml, p=0.031). Unlike in controls, no significant differences in sHLAG levels were observed among patients grouped by 14pb genotype. Thus, in a substantial number of late RA patients, the circulating sHLA-G molecules are impaired regarding LILRB1 recognition, meaning that although increased levels are observed; these molecules are not qualified to exert their protective functions against inflammation. Our findings offer new insights into the immunopathology of RA patients with long-lasting anti-RA-treatment and highlight the importance to also measure the binding capability of sHLA-G to LILRB1. | en |
dc.format.mimetype | application/pdf | pt_BR |
dc.language.iso | eng | pt_BR |
dc.relation.ispartof | Plos one. San Francisco. Vol. 10, no. 4 (Apr. 2015), e0123838, 14 p. | pt_BR |
dc.rights | Open Access | en |
dc.subject | Artrite reumatóide | pt_BR |
dc.subject | Polimorfismo genético | pt_BR |
dc.subject | Antígenos HLA-G | pt_BR |
dc.subject | Receptor B1 de leucócitos semelhante a imunoglobulina | pt_BR |
dc.title | The paradox of high availability and low recognition of soluble HLA-G by LILRB1 receptor in rheumatoid arthritis patients | pt_BR |
dc.type | Artigo de periódico | pt_BR |
dc.identifier.nrb | 001066289 | pt_BR |
dc.type.origin | Estrangeiro | pt_BR |
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