title: Th1 and Th2 polymorphisms in Sjögren's syndrome and rheumatoid arthritis.
abstract: BACKGROUND
  Sjogren's syndrome is characterized by T-cell infiltration of exocrine glands leading to parenchymal destruction and impaired glandular function. This process is orchestrated by cytokines, whose secretion can be regulated by genetic polymorphisms.
  
  
  METHODS
  The aim of this study was to investigate the influence of interleukin-6 -174G/C, interleukin-10 -1082G/A, tumor necrosis factor-α -308G/A, interferon-γ +874A/T gene polymorphisms in (RA) and secondary Sjögren's syndrome (sSS). A study sample that comprised of 138 Brazilian patients was divided into three groups: RA (n = 66), sSS (n = 20), and healthy controls - C (n = 52). Patients were subjected to Schirmer's test, unstimulated salivary flow rate, biopsy of minor salivary glands, and serological tests for diagnosing SS. Genomic DNA was obtained from saliva samples and submitted to genotyping. The association between genotypes/alelle frequency and SS susceptibility was tested, as well as their association with clinical features of SS.
  
  
  RESULTS
  Tumor necrosis factorα (TNFα)-308GA polymorphisms differed significantly between AR, SS, and C patients (P = 0.008). IL-6 overall G carriers and TNFα A carriers had a higher risk of presenting SS (P = 0.021). IL-6 polymorphism distribution was also distinctive regarding lymphocytic infiltration at the minor salivary glands (P = 0.026) and Schirmer's test (P = 0.035).
  
  
  CONCLUSIONS
  These results suggest that IL-6 -174GC and TNFα-308GA gene polymorphisms are associated with susceptibility to SS. Additionally, IL-6 polymorphism could influence lymphocytic infiltration of salivary glands and diminish lachrymal gland function.
authors.affiliation: Oral Medicine Unit, Departamento de Clínica e Odontologia Preventiva, Universidade Federal de Pernambuco, Recife, Brazil.
authors.forename: Thayse Rodrigues
authors.initials: TR
authors.lastname: de Souza
authors.forename: Alessandra
authors.initials: A
authors.lastname: de Albuquerque Tavares Carvalho
authors.forename: Ângela Pinto
authors.initials: ÂP
authors.lastname: Duarte
authors.forename: Stephen R
authors.initials: SR
authors.lastname: Porter
authors.forename: Jair C
authors.initials: JC
authors.lastname: Leão
authors.forename: Luiz Alcino
authors.initials: LA
authors.lastname: Gueiros
mesh_terms: D000225:Adenine; D000328:Adult; D000368:Aged; D000974:Antibodies, Antinuclear / Q000097:blood; D001172:Arthritis, Rheumatoid / Q000235:genetics / Q000276:immunology*; D001324:Autoantigens / Q000097:blood; D016022:Case-Control Studies; D003596:Cytosine; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006147:Guanine; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics; D016753:Interleukin-10 / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010456:Peptides, Cyclic / Q000097:blood; D011110:Polymorphism, Genetic / Q000235:genetics*; D012217:Rheumatoid Factor / Q000097:blood; D012261:Ribonucleoproteins / Q000097:blood; D012463:Saliva / Q000378:metabolism; D012470:Salivary Glands, Minor / Q000473:pathology; D012636:Secretory Rate / Q000502:physiology; D012859:Sjogren's Syndrome / Q000235:genetics / Q000276:immunology*; D013941:Thymine; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*; D055815:Young Adult; D000097585:SS-B Antigen; D000099207:SS-A Antigen
chemical_list: D000225:Adenine; D000974:Antibodies, Antinuclear; D001324:Autoantigens; D003596:Cytosine; D006147:Guanine; D007371:Interferon-gamma; D016753:Interleukin-10; D015850:Interleukin-6; D010456:Peptides, Cyclic; D012217:Rheumatoid Factor; D012261:Ribonucleoproteins; D013941:Thymine; D014409:Tumor Necrosis Factor-alpha; D000097585:SS-B Antigen; D000099207:SS-A Antigen; C508609:IL10 protein, human; C508600:IL6 protein, human; C487763:cyclic citrullinated peptide
keywords: Sjögren's syndrome; cytokines, helper T cells; rheumatoid arthritis