Chloroquine Enhances the Number of IL‐10 Producing Cells and the Expression of B7‐2 and ICAM‐1 in In Vitro‐Cultured PBMC

Scandinavian Journal of Immunology - Tập 55 Số 4 - Trang 399-408 - 2002
Elisabeth Hugosson1,2, Anders Björkman2, Marita Troye‐Blomberg1
1The Department of Immunology, Stockholm University
2The Department of Infectious Diseases, Karolinska Hospital, Karolinska Institutet, Stockholm, Sweden

Tóm tắt

Chloroquine is prescribed as both an anti‐malarial and an anti‐inflammatory drug. However, its immuno‐modulating effects remain largely unclear. Previous studies have shown that chloroquine inhibits antigen‐induced proliferation, implying immuno‐suppressive effects. In this study, we examined whether the inhibition of the proliferation reflects changes in the surface molecules that are important for T‐cell activation and whether chloroquine affects the balance between pro‐ and anti‐inflammatory cytokines. Chloroquine elevated the expression of the costimulatory and adhesion molecules B7‐2 (CD86) and ICAM‐1 (CD54) in peripheral mononuclear cells (PBMC). An increased percentage of CD14+ cells was also observed, and within this cell population, an increase in ICAM‐1 expression was revealed by double‐staining experiments. Assessment of the frequencies of interleukin (IL)‐10 and interferon (IFN)‐γ‐producing cells in in vitro‐cultivated PBMCs showed that the ratio between pro‐ and anti‐inflammatory cytokines changed after exposure to chloroquine, favouring anti‐inflammatory immune responses. This effect was mainly because of increased frequencies of IL‐10‐producing cells and was seen with or without the presence of stimulating antigens or mitogens. Our findings indicate that chloroquine affects the direction of the lymphocyte stimulation towards an anti‐inflammatory response by affecting the antigen‐presenting cells (APC) and the balance between pro‐ and anti‐inflammatory cytokines, rather than generally inhibiting cytokine production.

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Thông tin xuất bản

Scandinavian Journal of Immunology

Tập 55 Số 4

399-408

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