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1.
Chinese Journal of Immunology ; (12): 976-978, 2017.
Article in Chinese | WPRIM | ID: wpr-616533

ABSTRACT

Objective:Rheumatoid arthritis(RA) is a systemic autoimmune disease,but its etiology is unclear.Therefore,it is urgent to search antigens which is relate to induce this disease,however,there are few reports about the new self-antigens at home and abroad.In this study,we investigate new autoantigen through cloning.Methods: We used antigens in synovium of patients with rheumatoid arthritis as probe,extracted mRNA from synoviocyte,performed cDNA library immunological screening and sequence,and analyzed the conformation and performed Northern blotting.Results: We found that new autoantigen had 36.5% homology with retinoblastoma binding protein 1(RBP1)and it was found that these special protein structure such as AT-rich interaction domain,chromo domain,A+T-hook and TAF homology domain.Therefore,it will be named RBP1-like Protein(Rbik).Rbik RNA is not only expressed in the synovial membrane,but also in the heart,small intestine,muscle and other organs.Conclusion: We report that the discovery of the new autoantibodies to RBP1-like Protein(Rbik)may provide a new possible index and target in diagnosis and therapy.

2.
Chinese Journal of Immunology ; (12): 1309-1314,1318, 2016.
Article in Chinese | WPRIM | ID: wpr-604713

ABSTRACT

Objective:To clarify whether IL-10 enhanced the M2 phenotype induced by IL-4.Methods:M-CSF induced bone marrow-derived macrophages ( BMDMs) were generated from C57BL/6J mice bone marrow cells.The RNA transcriptional profile was e-valuated using the Mouse Whole Genome.We performed in vitro eosinophil migration assay and in vivo macrophage transfer.Results:The results showed that IL-10 enhanced gene expression of M2a markers induced by IL-4 in M-CSF-induced BMDMs.Moreover,IL-4 and IL-10 synergistically induced CCL24 ( Eotaxin-2) production.Enhanced CCL24 expression was also observed in GM-CSF-induced BMDMs and zymosan-elicited,thioglycolate-elicited and naive peritoneal macrophages.CCL24 was a CCR3 agonist and an eosinophil chemoattractant.In vitro,IL-4+IL-10-stimulated macrophages produced a large amount of CCL24 and increased eosinophil migration, which was inhibited by anti-CCL24 antibody.IL-4+IL-10-stimulated ( but not IL-4 or IL-10 alone) macrophages transferred into the peritoneumof C57BL/6J mice increased eosinophil infiltration into the peritoneal cavity.Conclusion:These results demonstrate that IL-4+IL-10-simulated macrophages have enhanced M2a macrophage-related gene expression,CCL24 production and eosinophil infiltration-inducing activity,thereby suggesting theircontribution to eosinophil-related diseases.

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