IL-7 induces human lymphokine-activated killer cell activity and is regulated by IL-4

• Published in: The Journal of immunology (1950) Vol. 146; no. 1; pp. 150 - 155
• Main Authors: Stotter, H, Custer, MC, Bolton, ES, Guedez, L, Lotze, MT
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 01.01.1991; American Association of Immunologists
• Subjects: Analysis of the immune response. Humoral and cellular immunity; Antigens, CD - metabolism; Antigens, Differentiation, T-Lymphocyte - metabolism; Biological and medical sciences; Cell Adhesion Molecules - metabolism; Cytotoxicity, Immunologic; Dose-Response Relationship, Drug; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; Immunobiology; In Vitro Techniques; Intercellular Adhesion Molecule-1; Interleukin-4 - pharmacology; Interleukin-7 - pharmacology; Killer Cells, Lymphokine-Activated - immunology; Lectins, C-Type; Lymphocyte Activation - drug effects; Lymphokines, interleukins ( function, expression); Receptors, Interleukin-2 - metabolism; Regulatory factors and their cellular receptors; Time Factors; Human; Cell proliferation; Interleukin 7; Interleukin 4; Cell population; Induction; LAK cell; Cytokine; Immune regulation; Lymphocyte; Biological activity
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.146.1.150

Induction of lymphokine-activated killer (LAK) activity by IL-2 has been described and characterized as broadly cytolytic activity against both fresh and cultured tumors. rIL-7 in the absence of IL-2 also induces LAK activity in human cells. This activity is unique for IL-7, because it is not shared by other cytokines including IL-1, IL-4, IL-6, and TNF-alpha. IL-7 also induces either de novo or increased expression of the surface markers CD25 (Tac, IL-2R alpha-chain), CD54 (ICAM-1), Mic beta 1 (IL-2R beta-chain) and CD69 (early T cell activation Ag). IL-7-induced LAK activity is independent of IL-2 secretion, because it is not abrogated by IL-2 antisera. The LAK precursor responding to IL-7 stimulation is enriched in the null cell fraction as has been demonstrated for IL-2-induced LAK cells. TGF-beta and IL-4 interfere with generation of LAK activity by IL-7. Anti-IL-4 antiserum enhances IL-7-induced LAK activity and augments induction of surface marker expression by IL-7. This may be indirect evidence that IL-7 stimulation leads to induction of IL-4 activity. Our results describe the activation of mature lymphoid cells by IL-7. This and the previously described role of IL-7 in lymphohemopoiesis makes it a cytokine of potential therapeutic value for treatment of immunodeficiency states and possibly the immunotherapy of cancer.