Cytotoxic T lymphocyte-associated antigen-4 polymorphism in patients with rheumatic heart disease.


Düzgün N., Duman T., Haydardedeolu F., Tutkak H.

Tissue antigens, cilt.74, sa.6, ss.539-42, 2009 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 74 Sayı: 6
  • Basım Tarihi: 2009
  • Doi Numarası: 10.1111/j.1399-0039.2009.01347.x
  • Dergi Adı: Tissue antigens
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.539-42
  • Anahtar Kelimeler: Acute rheumatic fever, Cytotoxic T lymphocyte-associated antigen-4 49 A/G, Polymorphism, Rheumatic heart disease
  • Ankara Üniversitesi Adresli: Evet

Özet

Acute rheumatic fever (ARF) is a systemic inflammatory disease occurring as a consequence of an exaggerated immune response to group A, beta haemolytic streptococcal pharyngitis. The molecular mimicry between human target organs/tissues and specific components of the infectious organism leads to the development of autoimmune reactions and cardiac tissue damage in rheumatic heart disease (RHD). Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) is a negative regulator of T cell activation and proliferation during the immune response. CTLA-4 gene polymorphism has been shown to affect the inhibitory function of CTLA-4. We aimed to analyze the association of CTLA-4 gene locus at position 49 of exon 1 with susceptibility to ARF/RHD. This study included a total of 98 patients with RHD as a sequela of ARF, who fulfilled the revised classification criteria of Jones and 154 healthy unrelated controls. CTLA-4 +49 A/G polymorphism was genotyped by using PCR-RLFP technique. Data was analyzed by binary logistic regression models. The frequencies of GG, GA and AA genotypes were found to be 14%, 47% and 39%, respectively, in patients and 6%, 45% and 49%, respectively, in controls. The GG genotype was found to be significantly different between patients and controls (OR: 3.11; P = 0.016). GA and AA genotypes did not statistically differ between patients and controls. Our data showed a significant association of +49G /G polymorphism in a small patient group with RHD. © 2009 John Wiley & Sons A/S.