title: HTLV-I virological and histopathological analysis in two cases of anti-centromere-antibody-seropositive Sjögren's syndrome.
abstract: BACKGROUND
  The aim of this study was to show the clinical and pathological characteristics of anti-centromere-antibody (ACA)-seropositive Sjögren's syndrome (SS) in two anti-human T-cell leukemia virus type I (HTLV-I)-seropositive patients.
  
  
  METHODS
  One patient was an HTLV-I carrier whereas the other was diagnosed with HTLV-I-associated myelopathy (HAM). Background data including serum HTLV-I titers, viral loads, and cytokine profiles were recorded. Azocarmine with aniline blue (Azan)-Mallory staining and immunohistochemistry of the labial salivary glands (LSGs) and a muscle biopsy specimen from the HAM patient were performed.
  
  
  RESULTS
  Serum transforming growth factor beta (TGF-β), tumor necrosis factor alpha (TNF-α), and HTLV-I viral load were high in the HAM-SS patient compared with the HTLV-I carrier. Fibrous change in LSG was prominent in the HAM-SS patient. Although TGF-β expression was similar in the two patients, expression of HTLV-I-related proteins including p12, p28, group-specific antigen (GAG), and nuclear factor kappa-B (NF-κB) in the LSG were dominantly detected in the HAM-SS patient. Frequency of TGF-β staining in HTLV-I-seropositive SS patients without ACA, HTLV-I-seronegative SS patients with ACA, and HTLV-I-seronegative SS patients without ACA was lower than that of the previous two patients.
  
  
  CONCLUSIONS
  A high HTLV-I viral load in situ is supposed to promote the production of cytokines, especially TGF-β, resulting in the fibrous change of LSG in ACA-seropositive SS patients.
authors.affiliation: Unit of Translational Medicine, Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki, Nagasaki, 852-8501, Japan. nakamura_hideki911@yahoo.co.jp
authors.forename: Hideki
authors.initials: H
authors.lastname: Nakamura
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Horai
authors.forename: Ayuko
authors.initials: A
authors.lastname: Tokuyama
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Yoshimura
authors.forename: Hideki
authors.initials: H
authors.lastname: Nakajima
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Ichinose
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yamasaki
authors.forename: Tatsufumi
authors.initials: T
authors.lastname: Nakamura
authors.forename: Tomayoshi
authors.initials: T
authors.lastname: Hayashi
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kawakami
mesh_terms: D000974:Antibodies, Antinuclear / Q000097:blood*; D015415:Biomarkers / Q000378:metabolism; D002353:Carrier State; D002503:Centromere / Q000276:immunology*; D005260:Female; D005355:Fibrosis / Q000473:pathology; D015490:HTLV-I Infections / Q000097:blood / Q000150:complications* / Q000473:pathology*; D015368:Human T-lymphotropic virus 1 / Q000302:isolation & purification / Q000502:physiology; D006801:Humans; D008046:Lip; D008875:Middle Aged; D009061:Mouth Mucosa; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology; D012470:Salivary Glands, Minor / Q000378:metabolism / Q000473:pathology / Q000821:virology; D012859:Sjogren's Syndrome / Q000097:blood / Q000473:pathology* / Q000821:virology*; D016211:Transforming Growth Factor alpha / Q000097:blood; D016212:Transforming Growth Factor beta / Q000097:blood; D019562:Viral Load; D014764:Viral Proteins / Q000378:metabolism; D014987:Xerostomia / Q000175:diagnosis / Q000209:etiology
chemical_list: D000974:Antibodies, Antinuclear; D015415:Biomarkers; D016211:Transforming Growth Factor alpha; D016212:Transforming Growth Factor beta; D014764:Viral Proteins