Reduction of Serum Soluble CD26/Dipeptidyl Peptidase IV Enzyme Activity and Its Correlation with Disease Activity in Systemic Lupus Erythematosus

HIROSHI KOBAYASHI, OSAMU HOSONO, TSUNEYO MIMORI, HIROSHI KAWASAKI, NAM HOANG DANG, HIROTOSHI TANAKA, and CHIKAO MORIMOTO

ABSTRACT.

Objective. CD26 is the cell surface activation antigen with dipeptidyl peptidase IV (DPPIV) enzyme activity at the extracellular domain that is preferentially expressed on memory T cells and has a role in T cell immune responses. The soluble form of CD26 is present in serum and recombinant soluble CD26 (rsCD26) can enhance in vitro antigen-specific T cell responses. To determine the role of soluble CD26 (sCD26) in the pathophysiology of patients with systemic lupus erythematosus (SLE), we measured levels of sCD26 and its specific DPPIV activity in serum.

Methods. Serum sCD26 levels and DPPIV activity were measured by sandwich ELISA in 53 patients with SLE and 54 healthy controls. Serum sCD26 was identified by immunoprecipitation and immunoblot analysis. Expression of CD26 on T cells was analyzed by flow cytometry.

Results. Serum levels of sCD26 and its specific DPPIV activity were significantly decreased in SLE and were inversely correlated with SLE disease activity index score, but not with clinical variables or clinical subsets of SLE. Close correlation between sCD26/DPPIV and disease activity was observed in the longitudinal study.

Conclusion. Serum levels of sCD26 may be involved in the pathophysiology of SLE, and appear to be useful as a new disease activity measure for SLE. (J Rheumatol 2002;29:1858-66)

Key Indexing Terms:

SYSTEMIC LUPUS ERYTHEMATOSUS
SOLUBLE CD26
DIPEPTIDYL PEPTIDASE IV
DISEASE ACTIVITY

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From the Division of Clinical Immunology, Advanced Clinical Research Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan; Department of Lymphoma/Myeloma, MD Anderson Cancer Center, Houston, Texas, USA; and Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.

Supported by US National Institutes of Health grant AR33713; and by grants-in-aid from the Ministry of Education, Culture, Sports, Science and Technology, and from the Ministry of Health, Labor and Welfare, Japan.

H. Kobayashi, MD, PhD; O. Hosono, MD, PhD; H. Kawasaki, MD, PhD; H. Tanaka, MD, PhD, Associate Professor; C. Morimoto, MD, PhD, Professor, Division of Clinical Immunology, Advanced Clinical Research Center, The Institute of Medical Science, University of Tokyo; N.H. Dang, MD, PhD, Assistant Professor, Department of Lymphoma/Myeloma, MD Anderson Cancer Center; T. Mimori, MD, PhD, Assistant Professor, Department of Internal Medicine, Keio University School of Medicine.

Address reprint requests to Dr. C. Morimoto, Division of Clinical Immunology, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. E-mail: morimoto@ims.u-tokyo.ac.jp

Submitted August 21, 2001; revision accepted March 7, 2002.

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