Regulation of CCR5 expression and MIP-1α production in CD4+ T cells from patients with rheumatoid arthritis

Chrong-Reen Wang, Ming-Fei Liu

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Production of CCR5 expression and MIP-1α, a ligand of CCR5, by CD4+ T cells from patients with rheumatoid arthritis (RA) were studied. We analysed further the influence of IL-15 stimulation, CD40/CD40 ligand (CD40L) interaction and CCR5 promotor polymorphism. One hundred and fifty-five RA patients and another 155 age- and sex-matched healthy individuals were enrolled. Peripheral CD4+ and double negative (DN) T cells from patients had lower portions of CCR5, whereas synovial CD4+ and DN T cells showed a much higher CCR5 expression. IL-15 significantly up-regulated the expression of CCR5 on purified CD4+ T cells. CD40L expression on synovial CD4+ T cells was increased greatly in CCR5+ portions by IL-15. MIP-1α production by synovial CD4+ T cells was also enhanced by IL-15. Co-culture of CD40 expressing synovial fibroblasts with IL-15-activated synovial CD4+ T cells significantly increased MIP-1α production. Expression of CCR5 on patients' CD4+ T cells was not influenced by the promotor polymorphism of CCR5 gene. Taken together, these data suggest CCR5+CD4+ T cells infiltrate the inflamed synovium and IL-15 up-regulates CCR5 and CD40L expression further and enhance MIP-1α production in synovial CD4+ T cells. Production of MIP-1α by synovial fibroblasts is significantly increased by engagement of CD40 with CD40L. Synovial microenvironment plays a potential role in regulation of CCR5+CD4+ T cells in rheumatoid joints.

Original languageEnglish
Pages (from-to)371-378
Number of pages8
JournalClinical and Experimental Immunology
Volume132
Issue number2
DOIs
Publication statusPublished - 2003 May 1

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Rheumatoid Arthritis
Interleukin-15
T-Lymphocytes
CD40 Ligand
Fibroblasts
Synovial Membrane
Coculture Techniques
Up-Regulation
Joints
Ligands

All Science Journal Classification (ASJC) codes

  • Immunology

Cite this

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abstract = "Production of CCR5 expression and MIP-1α, a ligand of CCR5, by CD4+ T cells from patients with rheumatoid arthritis (RA) were studied. We analysed further the influence of IL-15 stimulation, CD40/CD40 ligand (CD40L) interaction and CCR5 promotor polymorphism. One hundred and fifty-five RA patients and another 155 age- and sex-matched healthy individuals were enrolled. Peripheral CD4+ and double negative (DN) T cells from patients had lower portions of CCR5, whereas synovial CD4+ and DN T cells showed a much higher CCR5 expression. IL-15 significantly up-regulated the expression of CCR5 on purified CD4+ T cells. CD40L expression on synovial CD4+ T cells was increased greatly in CCR5+ portions by IL-15. MIP-1α production by synovial CD4+ T cells was also enhanced by IL-15. Co-culture of CD40 expressing synovial fibroblasts with IL-15-activated synovial CD4+ T cells significantly increased MIP-1α production. Expression of CCR5 on patients' CD4+ T cells was not influenced by the promotor polymorphism of CCR5 gene. Taken together, these data suggest CCR5+CD4+ T cells infiltrate the inflamed synovium and IL-15 up-regulates CCR5 and CD40L expression further and enhance MIP-1α production in synovial CD4+ T cells. Production of MIP-1α by synovial fibroblasts is significantly increased by engagement of CD40 with CD40L. Synovial microenvironment plays a potential role in regulation of CCR5+CD4+ T cells in rheumatoid joints.",
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Regulation of CCR5 expression and MIP-1α production in CD4+ T cells from patients with rheumatoid arthritis. / Wang, Chrong-Reen; Liu, Ming-Fei.

In: Clinical and Experimental Immunology, Vol. 132, No. 2, 01.05.2003, p. 371-378.

Research output: Contribution to journalArticle

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