Anti-CD80 Monoclonal antibody, clone 27-20B2 [FITC]

Systemic lupus erythematosus (SLE) is a chronic disease with proven interactions between immune system components, including both humoral- and cell-mediated immunity, as well as co-stimulatory and inhibitory molecules such as CD40 and CD72. Here, we investigated CD40 and CD72 expression on B cells of SLE children and assessed their prognostic values. We conducted a preliminary case-control study in Mansoura University Children's Hospital, Egypt from September 2018 to January 2020 including 27 SLE children and 27 healthy controls. We assessed cases during initial flare and after remission. Flow cytometry analysis was carried out for all participants for CD40 and CD72 expression of B cells. During flare, SLE cases had statistically significant higher CD40 and lower CD72 expression in comparison with controls (p < 0.001). After remission, the number of CD40(+)B cells significantly decreased (p < 0.001), while the number of CD72(+)B cells significantly increased (p < 0.001) in comparison with flare. We reported non-significant positive correlations between CD40 expression and SLE Disease Activity Index (SLEDAI;p = 0.347 during flare andp = 0.653 after remission) and negative correlations between CD72 expression and SLEDAI (p = 0.34 during flare andp = 0.044 after remission). No significant differences were detected between renal histopathology classes with regard to CDs expression on B cells (p = 0.45 for CD40 andp = 0.63 for CD72). In conclusion, CD40(+)B cells and CD72(+)B cells could be considered as markers of paediatric SLE flare and remission, respectively.

Background and Aims Ischemia-reperfusion injury (IRI) represents a risk factor in liver transplantation (LT). We have shown that overexpression of heme oxygenase-1 (HO-1) mitigates hepatic IRI in LT recipients. Here, we hypothesized that human antigen R (HuR), the stabilizer of adenylate-uridylate (AU)-rich mRNAs, is required for hepatoprotection in LT. Approach and Results In an experimental arm, HuR/HO-1 protein expression was correlated with hepatic IRI phenotype. In anin vitroinflammation mimic model of hepatic warm IRI, induction of HuR/HO-1 and cytoplasmic localization following cytokine preconditioning were detected in primary hepatocyte cultures, whereas HuR silencing caused negative regulation of HO-1, followed by enhanced cytotoxicity. Using the HuR-inhibitor, we showed that HuR likely regulates HO-1 through its 3 ' untranslated region and causes neutrophil activation (CD69+/lymphocyte antigen 6 complex locus G [Ly6-G]). HuR silencing in bone marrow-derived macrophages decreased HO-1 expression, leading to the induction of proinflammatory cytokines/chemokines. RNA sequencing of HuR silenced transcripts underin vitrowarm IRI revealed regulation of genesthymus cell antigen 1 (THY1), aconitate decarboxylase 1 (ACOD1), andProstaglandin E Synthase (PTGES). HuR, but not hypoxia-inducible protein alpha, positively regulated HO-1 in warm, but not cold, hypoxia/reoxygenation conditions. HuR modulated HO-1 in primary hepatocytes, neutrophils, and macrophages under reperfusion. Adjunctive inhibition of HuR diminished microtubule-associated proteins 1A/1B light chain 3B (LC3B), a marker for autophagosome, under HO-1 regulation, suggesting a cytoprotective mechanism in hepatic IR. In a clinical arm, hepatic biopsies from 51 patients with LT were analyzed at 2 hours after reperfusion. Graft HuR expression was negatively correlated with macrophage (CD80/CD86) and neutrophil (Cathepsin G) markers. Hepatic IRI increased HuR/HO-1 expression and inflammatory genes. High HuR-expressing liver grafts showed lower serum alanine aminotransferase/serum aspartate aminotransferase levels and improved LT survival. Conclusions This translational study identifies HuR as a regulator of HO-1-mediated cytoprotection in sterile liver inflammation and a biomarker of ischemic stress resistance in LT.