Author
YU, P - UNIV. WISCONSIN-MADISON | |
SCHULER, L - UNIV. WISCONSIN-MADISON | |
REJMAN, J - UNIV. WISCONSIN-MADISON | |
CHEN, H - UNIV. WISCONSIN-MADISON | |
GOSINK, K - UNIV. WISCONSIN-MADISON | |
Kehrli Jr, Marcus | |
PELAN, LISA - IA STATE UNIV., AMES, IA | |
CZUPRYNSKI, C - UNIV. WISCONSIN-MADISON |
Submitted to: Meeting Abstract
Publication Type: Abstract Only Publication Acceptance Date: 11/6/1996 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Interleukin-1 (IL-1) is a key mediator in inflammation and the immune response that is produced by mononuclear phagocytes and other cells. Among its many biological activities, IL-1 plays a pivotal role in driving the proliferation and activation of lymphocytes. The IL-1 family consists of three ligands (IL-1alpha, IL-1beta, and the IL-1 receptor antagonist) and two receptors (type I and type II). Studies of IL-1 receptors (IL-1R) on human and rodent cells indicate that the type I IL-1R receptor, which is larger and has a long cytoplasmic tail, is the active receptor that mediates signal transduction. In contrast, the type II IL-1R is smaller, lacks a cytoplasmic tail, and acts as a "decoy" receptor on the cell-surface and when shed into the extracellular fluid. Previous results suggested that there may be a relationship between the stimulation of T-cells by either IL-1alpha or IL-1beta, and the type of T helper cells cytokine profile (TH1 versus TH2) that was expressed. There is also evidence that the biological responses elicited by IL-1 are, in turn, influenced by the TH cytokine profile. For example, human neutrophils incubated with the TH2 cytokine IL-4 substantially upregulate the type II IL-1R. |