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CCR3, CCR5, Interleukin 4, and Interferon-g Expression on Synovial and Peripheral T Cells and Monocytes in Patients with Rheumatoid Arthritis

RIIKKA NISSINEN, MARJATTA LEIRISALO-REPO, MINNA TIITTANEN, HEIKKI JULKUNEN, HANNA HIRVONEN, TIMO PALOSUO, and OUTI VAARALA

ABSTRACT.

Objective. To characterize cytokine and chemokine receptor profiles of T cells and monocytes in inflamed synovium and peripheral blood (PB) in patients with rheumatoid arthritis (RA) and other arthritides.

Methods. We studied PB and synovial fluid (SF) samples taken from 20 patients with RA and 9 patients with other arthritides. PB cells from 8 healthy adults were used as controls. CCR3, CCR5, and intracellular interferon-g (IFN-g) and interleukin 4 (IL-4) expression in CD8 and CD8– T cell populations and in CD14 cells were determined with flow cytometry.

Results. Expression of CCR5 and CCR3 by CD8–, CD8 T cells and CD14 monocytes was increased in SF compared to PB cells in patients with RA and other arthritides. The number of CD8 T cells spontaneously expressing IL-4 and IFN-g was higher in SF than in PB in RA patients. Spontaneous CCR5 expression was associated with intracellular IFN-g expression in CD8 T cells derived from SF in RA. In CD8– T cells the ratio of CCR5 /CCR3 cells was increased in patients with RA compared to patients with other arthritides. The number of PB CD8– T cells expressing IFN-g after mitogen stimulation was higher in controls than in patients. In PB monocytes the ratio of CCR5 /CCR3 cells was increased in patients with RA compared to patients with other arthritides and controls.

Conclusion. T cells and monocytes infiltrating joints in RA and in other arthritides showed increased activation of both type 1 and type 2 immune markers. More pronounced type 1 immune response in joints, shown as an increased CCR5/CCR3 ratio, was found in the patients with RA versus those with other arthritides. Monocytes but not T cells in PB showed increased activation in RA. (J Rheumatol 2003;30:1928-34)

Key Indexing Terms:

CHEMOKINE RECEPTORS
CYTOKINES
RHEUMATOID ARTHRITIS
SYNOVIAL FLUID


From the Department of Molecular Medicine and Department of Health and Functional Capacity, National Public Health Institute, Helsinki; Department of Medicine, Division of Rheumatology, Helsinki University Central Hospital, Helsinki; Department of Internal Medicine, Peijas Hospital, Vantaa; and Rheumatism Foundation Hospital, Heinola, Finland.

Supported by the Academy of Finland, Instrumentarium Research Foundation, and Rheumatism Foundation Hospital.

R. Nissinen, MSc, Department of Molecular Medicine and Department of Health and Functional Capacity, National Public Health Institute; M. Leirisalo-Repo, MD, Professor, Department of Medicine, Division of Rheumatology, Helsinki University Central Hospital; M. Tiittanen, MSc; O. Vaarala, MD, Professor, Department of Molecular Medicine, National Public Health Institute; H. Julkunen, MD, PhD, Department of Internal Medicine, Peijas Hospital; H. Hirvonen, MD, Rheumatism Foundation Hospital; T. Palosuo, MD, Professor, Department of Health and Functional Capacity, National Public Health Institute.

Address reprint requests to R. Nissinen, Department of Molecular Medicine, National Public Health Institute, Biomedicum, PO Box 104, 00251 Helsinki, Finland. E-mail: riikka.nissinen@ktl.fi

Submitted July 9, 2002; revision accepted February 13, 2003.




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