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Human NK cells may be divided into a CD56dimsubset and a CD56brightsubset. In peripheral blood, CD56dimNK cells dominate, whereas in lymph nodes, CD56brightNK cells are more common. In this study we show that CD56brightNK 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-α production by CD14+monocytes in a manner that is dependent on cell:cell contact Conversely, CD14+monocytes synergize with monokines to promote IFN-γ production by these NK cells. Again, this interaction is dependent on cell:celll contact The experiments show that CD56brightNK 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

Publication Date

15/11/2004

Volume

173

Pages

6418 - 6426