Anti-MBL2 polyclonal antibody

Activation of the complement system is initiated by the alternative, the classical, or the lectin pathway. As the complement system is involved in the pathophysiology of graft rejection after kidney transplantation, we investigated the possible role of mannose-binding lectin in kidney transplantation and the influence of human leukocyte antigen (HLA) immunization on this process. In a prospective study of 544 kidney transplant patients over a follow-up period of 5 years, low serum levels of this lectin at the time of transplantation were found to be significantly associated with decreased 5-year death-censored graft survival (hazard ratio 1.68). Subanalysis showed that this association was confined to non-HLA-immunized patients (hazard ratio 1.93). The strongest association was seen in non-HLA-immunized patients receiving a kidney from a deceased donor (hazard ratio 2.93). No significant association with mannose-binding lectin levels and graft survival were found in HLA-immunized patients. Variant MBL2 genotypes causing low mannose-binding lectin serum concentrations showed the same association pattern. Our findings demonstrate a clear protective role of mannose-binding lectin and thus innate immunity in maintaining kidney graft survival, but these are probably overruled by HLA immunization. Kidney International (2013) 83, 264-271; doi:10.1038/ki.2012.373; published online 21 November 2012

Objectives: In the first part of this study, we analyzed clinical factors associated with pediatric-onset systemic lupus erythematosus (SLE), and patient susceptibility to herpes zoster (HZ). In the second part of this study, we characterized MBL2 genotype polymorphisms in pediatric-onset SLE patients and their possible associations with HZ. Methods: This 10-year prospective cohort study compared pediatric-onset SLE patients from Taiwan with and without histories of HZ. By using 2 years as a standard interval, patients with early-onset and late-onset of HZ were compared. MBL2 gene polymorphisms in exon 1 at codon 54, and in the promoter at the position -221 and -550, were tested immediately after patient enrollment. Results: We initially enrolled 98 SLE patients, and analyzed complete clinical characteristics of 82 patients (35 patients with HZ, 47 patients without HZ). The incidence of HZ was higher in SLE patients who had methylprednisolone pulse therapy, cyclophosphamide pulse therapy, and received higher cumulative steroid dose (P < 0.05 for all 3). There were no significant associations of HZ with MBL2 genotype or serum level of mannose-binding lectin. Conclusions: Pediatric-onset SLE patients were highly susceptible to HZ, with an incidence of 35.7%. Patients given steroid, cyclophosphamide, and high cumulative steroid dose were more likely to have had HZ. Deficiency of serum mannose-binding lectin and MBL2 gene polymorphism were not associated with HZ.