Comparative study of the residues 63 and 67 on the HLA-B molecule in patients with Takayasu's Arteritis

• Published in: Immunology letters Vol. 96; no. 2; pp. 225 - 229
• Main Authors: Vargas-Alarcón, Gilberto, Hernández-Pacheco, Guadalupe, Soto, Maria Elena, Murguía, Luis Enrique, Pérez-Hernández, Nonanzit, Granados, Julio, Reyes, Pedro A.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 31.01.2005
• Subjects: Alleles; Amino Acid Substitution - genetics; Female; Gene Frequency; Genetic Markers; Genetic Predisposition to Disease; Genetic susceptibility; Glutamic Acid - genetics; HLA-B Antigens - genetics; HLA-B molecule; Humans; Major Histocompatibility Complex; Male; Mexico; Serine - genetics; Takayasu Arteritis - diagnosis; Takayasu Arteritis - genetics; Takayasu's Arteritis; Mexico; Major Histocompatibility Complex; Takayasu's Arteritis; HLA-B molecule; Genetic susceptibility; Alleles
• ISSN: 0165-2478; 1879-0542
• DOI: 10.1016/j.imlet.2004.08.009

Takayasu's Arteritis (TA) has been associated with the Major Histocompatibility Complex (MHC) genes; nevertheless, results in several populations have been heterogeneous. Studies both in Mexican and Asian populations suggest that residues at positions 63 (glutamic acid) and 67 (serine) of the HLA-B molecule could be the genetic markers for TA. In the present work, we analyzed the sequence of HLA-B alleles in 26 TA patients and 62 healthy controls. HLA-B subtyping analysis showed that all B52 alleles were B*5201, whereas only one HLA-B39 allele was B*3902. Sequencing of HLA-B alleles showed that 19 out of 26 patients studied (73.0%) presented at least an allele with glutamic acid at position 63 and serine at position 67. This condition was observed in only 21.0% of the healthy controls (pC = 0.00001, OR = 10.23). Out of the seven remaining patients, one presented glutamic acid at position 63 and four showed serine at position 67. Two patients (2/26 = 7.7%) and 24 healthy controls (24/62 = 38.7%) did not show similarity at the mentioned positions (pC = 0.016, OR = 0.13). These data corroborate the participation of positions 63 and 67 in the genetic susceptibility to TA and explain the high heterogeneity of alleles associated with the disease in several populations.