title: Cytokine messenger RNA expression in the labial salivary glands of patients with Sjögren's syndrome.
abstract: OBJECTIVE
  To characterize the initiation and progress of localized autoimmune damage in Sjögren's syndrome (SS), an autoimmune disease that is also considered to be a lymphoaggressive disorder, by examining the pattern of cytokine production at the site of autoimmune damage.
  
  
  METHODS
  Using a polymerase chain reaction-based method, cytokine messenger RNA (mRNA) expression in the labial salivary glands of 15 patients with SS was investigated. In addition, the infiltrating lymphocytes in the labial salivary glands were examined immunohistochemically.
  
  
  RESULTS
  Messenger RNAs of Th1 cytokines, such as interleukin-2 (IL-2) and interferon-gamma, were consistently detected in all patients, while Th2 cytokine mRNAs, such as IL-4 and IL-5, were detected in some cases, in association with strong B cell accumulation in the labial salivary glands. Other cytokine mRNAs produced by a variety of cell types, including IL-10, IL-6, and transforming growth factor beta (TGF beta), were also consistently detected in all patients, while IL-12 mRNA was detected in some of the patients.
  
  
  CONCLUSIONS
  These results suggest that Th1 cytokines, as well as IL-10, IL-6, and TGF beta, are essential in the induction and/or maintenance of SS, while Th2 cytokines are involved in the progression of the disease process, especially local B cell activation.
authors.affiliation: Kyushu University, Fukuoka, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ohyama
authors.forename: S
authors.initials: S
authors.lastname: Nakamura
authors.forename: G
authors.initials: G
authors.lastname: Matsuzaki
authors.forename: M
authors.initials: M
authors.lastname: Shinohara
authors.forename: A
authors.initials: A
authors.lastname: Hiroki
authors.forename: T
authors.initials: T
authors.lastname: Fujimura
authors.forename: A
authors.initials: A
authors.lastname: Yamada
authors.forename: K
authors.initials: K
authors.lastname: Itoh
authors.forename: K
authors.initials: K
authors.lastname: Nomoto
mesh_terms: D000328:Adult; D000368:Aged; D001483:Base Sequence; D015415:Biomarkers; D001706:Biopsy; D002999:Clone Cells / Q000276:immunology; D016207:Cytokines / Q000235:genetics*; D018076:DNA, Complementary / Q000235:genetics; D005260:Female; D015870:Gene Expression / Q000276:immunology; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics; D016753:Interleukin-10 / Q000235:genetics; D018664:Interleukin-12 / Q000235:genetics; D007376:Interleukin-2 / Q000235:genetics; D015847:Interleukin-4 / Q000235:genetics; D015848:Interleukin-5 / Q000235:genetics; D015850:Interleukin-6 / Q000378:metabolism; D008046:Lip; D008875:Middle Aged; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D012470:Salivary Glands, Minor / Q000276:immunology*; D012859:Sjogren's Syndrome / Q000235:genetics*; D013601:T-Lymphocytes / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000235:genetics
chemical_list: D015415:Biomarkers; D016207:Cytokines; D018076:DNA, Complementary; D007376:Interleukin-2; D015848:Interleukin-5; D015850:Interleukin-6; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D016753:Interleukin-10; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma