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Rheumatology Advance Access originally published online on March 1, 2005
Rheumatology 2005 44(6):819-820; doi:10.1093/rheumatology/keh582
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

LETTER TO THE EDITOR

A role for TARC/CCL17, a CC chemokine, in New Zealand mice

H. Okamoto, H. Nishimura1 and N. Kamatani

Institute of Rheumatology, Tokyo Women's Medical University, Tokyo and 1 Toin Human Science and Technology Center, Department of Material Science and Technology, Toin University of Yokohama, Yokohama, Japan

Correspondence to: H. Okamoto, Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku, Tokyo 162-0054, Japan. E-mail: hokamoto@ior.twmu.ac.jp

The first 10% of the full text of this article appears below.

SIR, Systemic lupus erythematosus (SLE) is an autoimmune disease in which peripheral helper T2 (Th2) cells have traditionally been considered to predominate. However, contradicting results regarding helper T1 (Th1) predominance in SLE have recently been reported, so the issue of Th1 vs Th2 predominance in SLE patients remains unresolved. To clarify this matter, we have recently published data demonstrating that the plasma levels of thymus- and activation-regulated chemokine (TARC)/CCL17 . . . [Full Text of this Article]


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