T cell induction of membrane IL 1 on macrophages

• Published in: The Journal of immunology (1950) Vol. 137; no. 12; pp. 3868 - 3873
• Main Authors: Weaver, CT, Unanue, ER
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15-12-1986; American Association of Immunologists
• Subjects: Analysis of the immune response. Humoral and cellular immunity; Animals; Biological and medical sciences; Cell Communication; Concanavalin A - pharmacology; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Histocompatibility Antigens Class II - immunology; Immunobiology; Interleukin-1 - biosynthesis; Kinetics; Lymphokines - secretion; Lymphokines, interleukins ( function, expression); Macrophages - drug effects; Macrophages - metabolism; Membrane Proteins - biosynthesis; Mice; Mice, Inbred Strains; Protein Biosynthesis; Receptors, Antigen, T-Cell - immunology; Regulatory factors and their cellular receptors; T-Lymphocytes, Helper-Inducer - physiology; Soluble factor; Induction; Rodentia; Monokine; Vertebrata; Cell contact; Mammalia; Mouse; Animal; Interleukin 1; T-Lymphocyte; Plasma membrane; Macrophage
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.137.12.3868

We have studied the role of T cells in the induction of a membrane-associated form of interleukin 1 (mIL 1) in murine macrophages. T helper cell clones and a T cell hybridoma induced macrophages to express mIL 1 after an antigen-specific, Ia-restricted interaction. Induction of mIL 1 was proportional to antigen concentration and was increased in the early course of the response in macrophages pretreated in culture with interferon-gamma. mIL 1 activity was detectable 4 hr after interaction with T cells. mIL 1 induction was inhibited by antibodies to either class II molecules or the T cell receptor. Two pathways of T cell-mediated mIL 1 induction could be defined. In the first, T cells, whose protein synthesizing capacity was completely eliminated by pretreatment with the irreversible protein synthesis inhibitor emetine, induced levels of mIL 1 expression indistinguishable from controls. In the second, T cells stimulated by paraformaldehyde-fixed macrophages in the presence of concanavalin A or antigen secreted a soluble factor that induced macrophage mIL 1 expression. Thus, it appears that T cells may induce macrophages to express mIL 1 both by direct cell-cell contact mediated through binding of T cell receptor to the Ia/antigen complex, and through the release of a lymphokine after activation. This lymphokine does not appear to be IL 2, IFN-gamma, BSF-1, or CSF-1.