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Human NK cells may be divided into a CD56(dim) subset and a CD56(bright) subset. In peripheral blood, CD56(dim) NK cells dominate, whereas in lymph nodes, CD56(bright) NK cells are more common. In this study we show that CD56(bright) NK cells accumulate within inflammatory lesions in a wide variety of clinical diseases affecting several different anatomical sites. We demonstrate that when activated by the monokines IL-12, IL-15, and IL-18, these NK cells promote TNF-alpha production by CD14(+) monocytes in a manner that is dependent on cell:cell contact. Conversely, CD14(+) monocytes synergize with monokines to promote IFN-gamma production by these NK cells. Again, this interaction is dependent on cell:cell contact. The experiments show that CD56(bright) NK cells accumulate in inflammatory lesions and, in the appropriate cytokine environment, can engage with CD14(+) monocytes in a reciprocal activatory fashion, thereby amplifying the inflammatory response. Such a positive feedback loop is likely to be important in the pathogenesis of chronic inflammatory conditions such as rheumatoid arthritis.

Original publication

DOI

10.4049/jimmunol.173.10.6418

Type

Journal article

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Date

11/2004

Volume

173

Pages

6418 - 6426

Addresses

Division of Medicine, Imperial College London, Commonwealth Building, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.

Keywords

Killer Cells, Natural, Lymphocyte Subsets, Monocytes, Cells, Cultured, Humans, Arthritis, Rheumatoid, Inflammation, Cytokines, Coculture Techniques, Immunophenotyping, Lymphocyte Activation, Cell Communication, Cell Aggregation, Organ Specificity, Macrophage Activation, Interferon-gamma, Lipopolysaccharide Receptors, CD56 Antigen