Production of natural killer cell activity‐augmenting factor (interleukin‐6) by human epiphyseal chondrocytes

Abstract

Objective. We sought to determine the capacity of human epiphyseal chondrocytes to modulate the cytotoxic activity of human natural killer (NK) cells by determining whether they release interleukin-6 (IL-6), a cytokine recently shown to stimulate NK cell activity.Methods. Conditioned medium from human epiphyseal chondrocyte cultures (Ch-CM) was tested for IL-6 activity using the B9 cell hybridoma assay. Its NK cell-stimulating capacity in the presence of K562 (myelogenous leukemia) cells or human chondrocytes was evaluated in a 4-hour 51Cr-release assay. Ch-CMderived ILd/NK cell-augmenting factor activity was partially purified by high-performance liquid chromatography (HPLC) gel filtration and Western blot.Results. Ch-CM contained an NK cell-augmenting factor (NKAF) which was blocked by IL-2 or IL-6 antibodies. Ch-CM did not contain detectable IL-2 activity, but it stimulated IL-2 production by human

Toll‐like receptors and chondrocytes: The lipopolysaccharide‐induced decrease in cartilage matrix synthesis is dependent on the presence of toll‐like receptor 4 and antagonized by bone morphogenetic protein 7

“…However, TLRs not only are expressed by cells involved in activation of the immune system, but also have been found, among other molecules, in human aortic endothelial cells, lung epithelial cells, hepatocytes, and synoviocytes (36)(37)(38)(39). The observations reported herein, that TLRs are also expressed in articular chondrocytes, expand these findings and are consistent with the notion that these cells display functional properties in common with monocytes/macrophages (40)(41)(42)(43)(44)(45).…”

Differences in Synovial Fluid Levels of Matrix Metalloproteinases Suggest Separate Mechanisms of Pathogenesis in Lyme Arthritis before and after Antibiotic Treatment

“…Chondrocytes display many functional properties in common with cells of monocyte/macrophage lineage, including production of immunoregulatory cytokines, release of reactive oxygen intermediates, stimulation of autologous and allogenic mixed leukocyte reactions, and the ability to function as antigen-presenting cells [29][30][31][32][33][34]. Chondrocytes also share expression of many surface antigens with monocytes and/or macrophages [23].…”

Mechanism of longitudinal bone growth and its regulation by growth plate chondrocytes

“…1968; Brighton et al, 1973;Fell, 1925;Hanaoka, 1976;Morris and Appleton, 1984;Oi and Utsumi, 1980;Shimomura, 1973; van der Stricht, 18901, and the various proposals include degeneration (Brighton et al, 1973;Farnum and Wilsman, 1987;Fell, 19251, active cell killing (Kay, 1981;Lance, 1989;MacDermott et al, 1985;Malejczyk et al, 1992;Perez et al, 1990;Simpsoni, 1981;Young and Cohn, 1986), and transformation into osteoblasts (Crelin and Koch, 1967;Holtrop, 1966;Roach, 1992;Rohr, 1963;Thesingh et al, 1991;van der Stricht, 1890) or mesenchymal cells (Brachet, 1893;Fell, 1928;Hanaoka, 1976). That terminal chondrocytes may be actively destroyed, rather than dying a natural death, is a relatively recent, but hypothetical, conception (Hunziker et al, 1984;Kay, 1981;Lance, 1989;MacDermott et al, 1985;Malejczyk et al, 19921, although the idea that such a mechanism exists has been proposed for cells in a number of different tissues (Perez et al, 1990;Simpsoni, 1981;Young and Cohn, 1986).…”