IL-6 is an intermediate in IL-1-induced thymocyte proliferation

• Published in: The Journal of immunology (1950) Vol. 142; no. 12; pp. 4335 - 4338
• Main Authors: Helle, M, Boeije, L, Aarden, LA
• Format: Journal Article
• Language: English
• Published: United States Am Assoc Immnol 15.06.1989
• Subjects: Adjuvants, Immunologic - pharmacology; Animals; Cell Separation; Centrifugation, Density Gradient; Drug Synergism; Interleukin-1 - pharmacology; Interleukin-2 - physiology; Interleukin-6; Interleukins - biosynthesis; Interleukins - pharmacology; Interleukins - physiology; Leukocyte Count; Lymphocyte Activation - drug effects; Mice; Mice, Inbred C3H; T-Lymphocytes - immunology; T-Lymphocytes - metabolism
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.142.12.4335

Both IL-1 and IL-6 have been shown to be comitogenic for lectin-stimulated thymocytes. Thymocytes cultured in the presence of IL-1 produce IL-6 themselves. This IL-6 production is caused by a cell population with low buoyant density. After removal of these cells, IL-6 or IL-2 are still co-mitogenic for thymocytes whereas IL-1 is not. Addition of IL-1 to such thymocytes renders them about 100-fold more sensitive to IL-6. At all conditions proliferation is inhibitable with antibodies to IL-2 and to the IL-2R. Our experiments show that IL-1-driven proliferation of thymocytes is dependent on endogenous IL-6 production and that in the classical thymocyte assay IL-1 has a dual role: it induces IL-6 production and it greatly increases the sensitivity for IL-6.