These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Interleukin 1-mediated activation of interleukin 4 (IL 4)-producing T lymphocytes. Proliferation by IL 4-dependent and IL 4-independent mechanisms.
    Author: Ho SN, Abraham RT, Nilson A, Handwerger BS, McKean DJ.
    Journal: J Immunol; 1987 Sep 01; 139(5):1532-40. PubMed ID: 3114369.
    Abstract:
    The role of IL 1 in the activation of IL 4-producing murine T cell clones was investigated by using a calcium ionophore (ionomycin) or a phorbol ester (12-O-tetradecanoylphorbol 13-acetate; TPA) as T cell receptor-independent costimuli. The use of these pharmacologic agents to investigate IL 1-mediated T cell activation revealed two distinct mechanisms of activation. IL 1 in combination with ionomycin (iono/rIL 1) stimulated a proliferative response that was associated with the production of IL 4 as measured by lymphokine bioassay and mRNA studies. Furthermore, inhibition of this proliferative response with an anti-IL 4 monoclonal antibody or cyclosporine indicated that IL 4 functions as an autocrine growth factor. In contrast, IL 1 synergized with TPA (TPA/rIL 1) to induce proliferation in the absence of either IL 4 or IL 2 gene transcription or lymphokine secretion. The IL 4-independence of this activation mechanism was further supported by the failure of both anti-IL 4 antibodies and cyclosporine to inhibit the response. In addition, activation by TPA/rIL 1 caused no detectable alteration in cytoplasmic calcium levels. Both IL 4-dependent and IL 4-independent activation responses were associated with the expression of functional receptors for IL 2 as well as IL 4. Characterization of these activation responses suggests that the synergistic activity of IL 1 during T cell activation is multipotential. The nature of an IL 1-dependent T cell growth response, therefore, may vary depending on the balance of intracellular signals generated concurrently through the T cell receptor complex and other regulatory surface molecules.
    [Abstract] [Full Text] [Related] [New Search]