PMID- 22526828
OWN - NLM
STAT- MEDLINE
DCOM- 20130613
LR  - 20161020
IS  - 1439-7609 (Electronic)
IS  - 1439-7595 (Linking)
VI  - 23
IP  - 1
DP  - 2013 Jan
TI  - HTLV-I virological and histopathological analysis in two cases of 
      anti-centromere-antibody-seropositive Sjogren's syndrome.
PG  - 133-9
LID - 10.1007/s10165-012-0641-x [doi]
AB  - INTRODUCTION: The aim of this study was to show the clinical and pathological 
      characteristics of anti-centromere-antibody (ACA)-seropositive Sjogren'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-beta), tumor necrosis 
      factor alpha (TNF-alpha), 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-beta 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-kappaB) in the LSG were dominantly detected in 
      the HAM-SS patient. Frequency of TGF-beta 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. CONCLUSION: A high HTLV-I viral load in situ is supposed to promote 
      the production of cytokines, especially TGF-beta, resulting in the fibrous change of 
      LSG in ACA-seropositive SS patients.
FAU - Nakamura, Hideki
AU  - Nakamura H
AD  - 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
FAU - Horai, Yoshiro
AU  - Horai Y
FAU - Tokuyama, Ayuko
AU  - Tokuyama A
FAU - Yoshimura, Shunsuke
AU  - Yoshimura S
FAU - Nakajima, Hideki
AU  - Nakajima H
FAU - Ichinose, Kunihiro
AU  - Ichinose K
FAU - Yamasaki, Satoshi
AU  - Yamasaki S
FAU - Nakamura, Tatsufumi
AU  - Nakamura T
FAU - Hayashi, Tomayoshi
AU  - Hayashi T
FAU - Kawakami, Atsushi
AU  - Kawakami A
LA  - eng
PT  - Case Reports
PT  - Journal Article
DEP - 20120418
PL  - England
TA  - Mod Rheumatol
JT  - Modern rheumatology
JID - 100959226
RN  - 0 (Antibodies, Antinuclear)
RN  - 0 (Biomarkers)
RN  - 0 (Transforming Growth Factor alpha)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Antibodies, Antinuclear/*blood
MH  - Biomarkers/metabolism
MH  - Carrier State
MH  - Centromere/*immunology
MH  - Female
MH  - Fibrosis/pathology
MH  - HTLV-I Infections/blood/*complications/*pathology
MH  - Human T-lymphotropic virus 1/isolation & purification/physiology
MH  - Humans
MH  - Lip
MH  - Middle Aged
MH  - Mouth Mucosa
MH  - Muscle, Skeletal/metabolism/pathology
MH  - Salivary Glands, Minor/metabolism/pathology/virology
MH  - Sjogren's Syndrome/blood/*pathology/*virology
MH  - Transforming Growth Factor alpha/blood
MH  - Transforming Growth Factor beta/blood
MH  - Viral Load
MH  - Viral Proteins/metabolism
MH  - Xerostomia/diagnosis/etiology
EDAT- 2012/04/25 06:00
MHDA- 2013/06/14 06:00
CRDT- 2012/04/25 06:00
PHST- 2012/01/27 00:00 [received]
PHST- 2012/03/22 00:00 [accepted]
PHST- 2012/04/25 06:00 [entrez]
PHST- 2012/04/25 06:00 [pubmed]
PHST- 2013/06/14 06:00 [medline]
AID - 10.1007/s10165-012-0641-x [doi]
PST - ppublish
SO  - Mod Rheumatol. 2013 Jan;23(1):133-9. doi: 10.1007/s10165-012-0641-x. Epub 2012 
      Apr 18.