Polymorphisms of Fcγlla receptors in Chilean patients with systemic lupus erythematosus

Flavio Carrión A, Fernando Figueroa E, M. Eugenia Martínez R, Loreto Massardo V, Tamara Pérez G, Carolina Foster B, Cecilia Mancilla M, Oscar Neira Q, Leonardo Guzmán B, Viviana Valenzuela M, Ramón Urrutia L, Sergio Carmona G, Maximiliano Figueroa, Alessandra Lubiano A, Eduardo Wainstein G

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Resumen

Background: Polymorphisms of Fc receptors for IgG (FcγR) have been proposed as a genetic factor that influences susceptibility for systemic lupus erythematosus (SLE). Human FćRIIa has 2 codominantly expressed alleles, H131 and R131, which differ at amino acid position 131 in the second extracelular domain (histidine or arginine respectively) and differ substantially in their ability to hind human IgG2. The H131 allele binds IgG2 efficiently, whereas R131 hinds it poorly. Because IgG2 is a poor activator of the classical complement pathway, the H131 is essential for the disposal of IgG2 immune complexes. Aim: To determine the distribution of FcγRIIA genes in a cohort of Chilean SLE patients, with or without a history of lupus nephritis. Patients and methods: We studied 52 Chilean SLE patients fulfilling the 1982 American College of Rheumatology (ACR) criteria, 20 of whom had a history of nephritis, and 44 ethnically matched disease-free controls. FcγRIIa allotypes were genotyped by PCR. Results: No significant association was observed between the low affinity FcγRII receptor (FcgRIIa-R131) and the presence of SLE or lupus nephritis. However, genotype frequencies in SLE patients but not in controls, departed from the proportions predicted by the Hardy-Weinberg equilibrium, suggesting this locus might be related to the disease. Conclusions: Our results suggest that in Chilean patients with SLE, as well as in many other populations, the R131 allotype is not a major factor predisposing to the development of SLE or lupus nephritis.
Idioma originalInglés estadounidense
Páginas (desde-hasta)11-18
Número de páginas8
PublicaciónRevista Medica de Chile
Volumen131
N.º1
EstadoPublicada - 1 ene. 2003

Palabras clave

  • Lupus erythematosus, systemic
  • Lupus nephritis
  • Receptors, IgG

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