Molecular features of CD71 expression in renal tissue in IgA nephropathy
- VernacularTitle:IgA肾病肾组织中CD71表达的分子特征
- Author:
Aiping ZHANG
;
Ziliang WANG
;
Yanxia WANG
- Publication Type:Journal Article
- Keywords:
glomerulonephritis,IgA;
receptors,transferrin;
biopsy,needle
- From:
Medical Journal of Chinese People's Liberation Army
2001;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the molecular pathologic features of CD71 and the correlation between CD71 expression and IgA deposit in IgA nephropathy(IgAN),and to investigate the role of CD71 in pathogenesis of IgAN in order to direct the therapeutic strategies.Methods According to clinical manifestations and pathological diagnosis,170 cases of renal biopsy were divided into IgA deposition nephritis(primary group),non-IgAN with IgA deposition(secondary group)and no IgA deposited nephritis(control group).Immunofluorescence double-staining using TRITC-conjugated anti CD71 antibody and FITC-conjugated anti-human IgA antibody was performed to illustrate the expression of CD71 and IgA respectively by confocal microscopy.Results No CD71 expression was found in control group,while the CD71 was positively expressed in primary and secondary groups to various levels.The intensity of expression of CD71 in primary group was more intense than that in the secondary group.The expression of CD71 in the IgAN tissues correlated closely with the accumulation of IgA.CD71 and IgA were distributed in mesangial area and capillary lumina of glomeruli of IgAN(primary group).The study showed that CD71 expression and IgA deposition were co-localized under confocal fluorescence microscopy.Conclusion CD71 is highly expressed in the glomeruli of primary IgAN.The expression of CD71 in the IgAN tissues correlats closely with the accumulation of IgA.CD71 and IgA are co-localized under confocal fluorescence microscopy.The present study reveals that CD71 is one of IgA receptors and involves in the course of IgAN.The results suggests that CD71 may play an important role in immunopathogenesis of IgAN.
