RGD Reference Report - FcgammaRIIa-131R allele and FcgammaRIIIa-176V/V genotype are risk factors for progression of IgA nephropathy. - Rat Genome Database

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FcgammaRIIa-131R allele and FcgammaRIIIa-176V/V genotype are risk factors for progression of IgA nephropathy.

Authors: Tanaka, Y  Suzuki, Y  Tsuge, T  Kanamaru, Y  Horikoshi, S  Monteiro, RC  Tomino, Y 
Citation: Tanaka Y, etal., Nephrol Dial Transplant. 2005 Nov;20(11):2439-45.
RGD ID: 5508463
Pubmed: PMID:16221721   (View Abstract at PubMed)
DOI: DOI:10.1093/ndt/gfi043   (Journal Full-text)

BACKGROUND: Fcgamma receptors (FcgammaRs) may play an important role in positive and negative regulation of immune cell responses and immune complex (IC) clearance. Mesangial IgG deposition and circulating IgG/IgA-IC in sera are observed in patients with IgA nephropathy (IgAN). Therefore, the pathological roles of IgG-IC in IgAN have been discussed. On the other hand, several studies have identified FcgammaR polymorphisms (FcgammaRIIa, FcgammaRIIIa and FcgammaRIIIb) that determine susceptibility to autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. The objective of the present study was to clarify whether FcgammaR polymorphisms influence susceptibility to IgAN, clinical features or severity in patients with IgAN. METHODS: Japanese patients with IgAN (n = 124) and healthy controls (n = 100) were genotyped for FcgammaR polymorphisms (FcgammaRIIa-131H or R, FcgammaRIIIa-176F or V and FcgammaRIIIb-NA1 or -NA2). The genotyping of these polymorphisms was performed using allele-specific polymerase chain reaction (PCR) methods. Associations among FcgammaR polymorphisms and susceptibility, age of onset, levels of serum immunoglobulins, intensity of glomerular IgG deposition and pathological severity were analysed. RESULTS: These three FcgammaR polymorphisms showed no significant differences in genotype and allele frequencies between the IgAN patients and healthy controls. Each FcgammaR polymorphism had no influence on age of onset, serum levels of IgG and glomerular IgG deposition in IgAN. However, FcgammaRIIa-131R (R/R or H/R) or FcgammaRIIIa-176V homozygous carriers (V/V) showed significantly more severe injury than FcgammaRIIa-131H homozygous (H/H) (P < 0.03) or FcgammaRIIIa-176F carriers (F/F or F/V) (P < 0.03), respectively. CONCLUSION: The present study shows that polymorphisms of FcgammaRIIa and FcgammaRIIIa influence the severity of IgAN in Japanese patients but not the incidence, suggesting that IgG-IC may play important roles in the progression and prognosis of this disease via FcgammaRs.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
FCGR3AHumanIgA glomerulonephritis disease_progressionIAGP DNA:polymorphism:exon:p.F176V(human)RGD 
Fcgr3aRatIgA glomerulonephritis disease_progressionISOFCGR3A (Homo sapiens)DNA:polymorphism:exon:p.F176V(human)RGD 
Fcgr4MouseIgA glomerulonephritis disease_progressionISOFCGR3A (Homo sapiens)DNA:polymorphism:exon:p.F176V(human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Fcgr3a  (Fc gamma receptor 3A)

Genes (Mus musculus)
Fcgr4  (Fc receptor, IgG, low affinity IV)

Genes (Homo sapiens)
FCGR3A  (Fc gamma receptor IIIa)


Additional Information