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Rheumatology Advance Access originally published online on May 20, 2009
Rheumatology 2009 48(7):854-855; doi:10.1093/rheumatology/kep072
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

LETTERS TO THE EDITOR

Low prevalence of ectopic germinal centre formation in patients with HTLV-I-associated Sjögren's syndrome

Hideki Nakamura1, Atsushi Kawakami1, Tomayoshi Hayashi2, Tatsufumi Nakamura3, Naoki Iwamoto1, Satoshi Yamasaki1, Hiroaki Ida1 and Katsumi Eguchi1

1Department of Immunology and Rheumatology, Unit of Translational Medicine, Nagasaki University Graduate School of Biomedical Sciences,2Department of Pathology, Nagasaki University Hospital and 3Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan

Correspondence to: Hideki Nakamura, Department of Immunology and Rheumatology, Unit of Translational Medicine, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki City, Nagasaki 852-8501, Japan. E-mail: nhideki@nagasaki-u.ac.jp

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SIR, We have proposed that HTLV-I infection can be a possible environmental factor for SS based on high prevalence of an anti-HTLV-I antibody in primary Sjögren's syndrome (pSS) in Nagasaki [1–3], and recently confirmed that labial salivary glands (LSGs) of the HTLV-I-seropositive SS patients are less damaged in radiography [4]. Amft et al. [5] revealed the prominent expression of B cell-attracting chemokine 1 (BCA-1/CXCL13) on endothelial cells and lymphocytic aggregates in the ectopic germinal centre (GC) of LSGs in SS, speculating that ectopic GC is associated with the autoantibodies production as well as the . . . [Full Text of this Article]


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