Lymphokine-mediated suppression of chondrocyte glycosaminoglycan and protein synthesis.
Spontaneously released and T cell mitogen augmented lymphokine produced by human mononuclear cells has been shown to induce a concentration dependent reversible suppression of chondrocyte glycosaminoglycan and protein synthesis without significantly enhancing chondrocyte catabolic activity. The modulatory factor(s) is of T cell origin and is trypsin, pronase, and heat sensitive. Prostaglandin inhibitors failed to influence factor formation or activity. Although eluting from Sephadex G-100 over a wide range, peak activity had an approximate molecular weight of 53,000 and appeared distinct from recognized forms of lymphotoxin.
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D002356:Cartilage / Q000166:cytology / Q000378:metabolism*; D002417:Cattle; D004798:Enzymes / Q000378:metabolism; D006025:Glycosaminoglycans / Q000037:antagonists & inhibitors*; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007376:Interleukin-2 / Q000494:pharmacology; D008222:Lymphokines / Q000096:biosynthesis / Q000494:pharmacology*; D008233:Lymphotoxin-alpha / Q000494:pharmacology; D008469:Meclofenamic Acid / Q000494:pharmacology; D014176:Protein Biosynthesis; D011506:Proteins / Q000037:antagonists & inhibitors; D011691:Puromycin / Q000494:pharmacology; D011817:Rabbits; D013997:Time Factors
D000596:Amino Acids; D004798:Enzymes; D006025:Glycosaminoglycans; D007376:Interleukin-2; D008222:Lymphokines; D008233:Lymphotoxin-alpha; D011506:Proteins; D008469:Meclofenamic Acid; D011691:Puromycin; D007213:Indomethacin