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Disease Markers
Volume 30, Issue 1, Pages 25-29
http://dx.doi.org/10.3233/DMA-2011-0760

Association of CD28 IVS3 +17T/C Polymorphism with Soluble CD28 in Rheumatoid Arthritis

I. Y. Ledezma-Lozano,1 J. J. Padilla-Martínez,1 S. D. Leyva-Torres,2 I. Parra-Rojas,3 M. G. Ramírez-Dueñas,4 Ana Laura Pereira-Suárez,4 H. Rangel-Villalobos,5 S. L. Ruiz-Quezada,6 P. E. Sánchez-Hernández,4 and J. F. Muñoz-Valle1

1Departamento de Biología Molecular y Genómica. Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico
2Department of Rheumatology. Hospital "Valentín Gómez-Farías ISSSTE", Zapopan, Jalisco, Mexico
3Unidad Académica de Ciencias Químico-Biológicas, Universidad Autónoma de Guerrero, Chilpancingo, Guerrero, Mexico
4Laboratorio de Inmunología. Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico
5Instituto de Investigación en Genética Molecular. Centro Universitario de la Ciénega, Universidad de Guadalajara; Ocotlán, Jalisco, Mexico
6Laboratorio de Biología Molecular, Centro Universitario de Ciencias Exactas e Ingenierías, Universidad de Guadalajara; Guadalalajara, Jalisco, Mexico

Received 14 April 2011; Accepted 14 April 2011

Copyright © 2011 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective: Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology in which inflammatory pathology involves T cell activation and the CD28 costimulatory molecule involved in T cell presentation. The gene includes the CD28 IVS3 +17T/C polymorphism that could be associated with susceptibility to RA whereas the soluble concentrations of CD28 (sCD28) could be related to clinical activity.

Methods: We investigated the CD28 IVS3 +17T/C polymorphism in 200 RA patients and 200 healthy subjects (HS). Furthermore, we quantified the sCD28 concentrations in 77 samples of each group. We applied indexes focused to determine the activity and disability (DAS28 and Spanish HAQ-DI, respectively) in RA patients.

Methods: We investigated the CD28 IVS3 +17T/C polymorphism in 200 RA patients and 200 healthy subjects (HS). Furthermore, we quantified the sCD28 concentrations in 77 samples of each group. We applied indexes focused to determine the activity and disability (DAS28 and Spanish HAQ-DI, respectively) in RA patients.

Results: RA patients had significantly higher frequencies of the CD28 T allele compared to HS (p = 0.032 OR = 1.59, C.I. 1.02–2.49). In addition, the IVS3 +17 T/T genotype frequency was also increased in RA vs. HS (p = 0.026). The RA patients showed higher sCD28 serum levels than HS (p = 0.001). Carriers of the T/T genotype in RA patients showed higher sCD28 levels than C/C carriers (p = 0.047). In addition, a correlation between sCD28 and Spanish HAQ-DI (correlation, 0.272; p = 0.016), was found.

Conclusion: The T allele in CD28 IVS3 +17T/C polymorphism is associated with a susceptibility to RA in Western Mexico. In addition, increased sCD28 levels are related to T/T genotype in RA patients.