Anti-IL23A polyclonal antibody

Objective. The aim of this study was to assess the possible association between the interleukin-12B (IL12B) and interleukin-12 receptor beta 1 (IL12RB1) gene polymorphisms with systemic lupus erythematosus (SLE). In addition, we have undertaken a systematic search for genetic variants of interleukin 23 (IL23A). Methods. The study was conducted on 559 SLE patients and 603 ethnically matched healthy controls. Genotyping of the IL12B [IL12Bpro and IL12B 3' untranslated region (UTR)] and IL12RB1 (641A -> G, 1094T -> C and 1132G -> C) polymorphisms was performed with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR-fluorescent methods, whereas IL23A genetic variants were realized with direct sequencing. Results. No statistically significant differences in the distribution of the IL12B and the IL12RB1 genotypes and alleles were observed when comparing SLE patients and control subjects. Additionally, no differences in the genotype and allele distribution were found when SLE patients were stratified according to the presence or absence of lupus nephritis. Despite an extensive analysis in 30 individuals, variations located in the exons and in the 5' and 3' UTR regions of IL23A gene were not found in any case. Conclusions. These results suggest that polymorphisms located in IL12B, IL12RB1 and IL23A genes may not play a relevant role in the susceptibility or severity of SLE in the Spanish population.

Background: Ankylosing spondylitis (AS) is an auto-inflammatory debilitating disorder with a complex pathogenesis. The adenosinergic pathway is an immunologic regulating pathway with a potential role in AS pathophysiology. In the present study, we have aimed to investigate the influence of A(2A) adenosine receptor (A(2A)AR) activation on tumor necrosis factor-alpha (TNF-alpha) and interleukin-23 (IL-23) expression and secretion by monocyte-generated macrophages of AS patients. Methods: Whole-blood separated monocytes were extracted from 14 AS patients and 14 healthy controls. Macrophages were differentiated by macrophage colony-stimulating factor (M-CSF), and surface markers were confirmed by flow cytometer. Cells were treated with CGS-21680 as a known agonist of A(2A)AR. Analysis of ADORA2A, TNFA, and IL23A gene expression was performed by SYBR green real-time PCR. The concentration of secreted cytokines was also measured by ELISA kits. Results: Based on our analysis, CGS-21680 significantly decreased TNF-alpha secretion by monocyte-derived macrophages of AS patients. Moreover, A(2A)AR agonist increased the IL23A mRNA expression level in monocyte-derived macrophages of AS patients considerably. Whereas, CGS-21680 did not have any influence on macrophages of healthy individuals. Conclusion: According to our results, it appears that A(2A)AR activation can increase IL-23 secretion by monocyte-derived macrophages of AS patients. Although the TNF-alpha reducing effect of A(2A)AR agonists can be a potential target in AS treatment, robust increasing of IL-23 should be considered as the undesirable effect of these agents.