hIL4/IL13 Dual Effector Reporter Cell

Interleukin-4 is produced mainly by a subpopulation of activated T-cells (Th2) that are the biologically most active helper cells for B-cells and that also secrete IL-5 and IL-6. The biological activities of IL-4 are mediated by a specific receptor. The extracellular domain of the IL-4 receptor is related to the receptors for EPO, IL-6, and the beta chain of the IL2 receptor (CD124). Two types of IL-4 receptor (IL-4R) exist: the type 1 receptor is a heterodimer consisting of CD132 and IL-4R-alpha. The type 2 receptor is a heterodimer consisting of IL-4Ralpha and IL-13Ralpha1. IL-4 enhances expression of MHC class 2 antigens on B-cells. It can promote their capacity to respond to other B-cell stimuli and to present antigens for T-cells. Pretreatment of macrophages with IL-4 prevents the production of IL1, TNF-alpha and prostaglandins in response to activation of the cells by bacterial endotoxins or IFN-gamma. IL-4 synergises with EPO and G-CSF in the generation of colonies containing granulocytes or erythroid progenitor cells in a colony formation assay.

Human IL-13 is expressed in activated T- helper cells (resembling Th0, Th1, Th2), and T-cells expressing CD8. The alpha chain of the IL1-3 receptor has weak binding activity for IL-13. High affinity receptors are formed when the receptor alpha chains of IL-13 and IL-4 receptors are coexpressed. The receptors for IL-13 and IL-4 share a common gamma subunit that is found also in the IL-2 receptor. Different IL-13 receptor structures have been shown to exist on various cell types and the IL-13 receptor may share more than one component with IL-4 receptor. IL-13 down-modulates macrophage activity, reducing the production of pro-inflammatory cytokines and chemokines in response to IFN-gamma or bacterial lypopolysaccharides. IL-13 enhances the production of the IL-1 receptor antagonist IL-1ra. IL-13 also decreases the production of nitric oxide by activated macrophages, leading to a decrease in parasiticidal activity. IL-13 induces differentiation of human monocytes, enhances survival time in culture, and also induces differentiation and proliferation and Isotype switching in B-cells.

Figure 1. Dose Response of Recombinant Human lL13 in Human hlL4/IL13 Dual Effector Reporter Cells.

Figure 2. Dose Response of Recombinant Human lL4 in hlL4/IL13 Dual Effector Reporter Cells (C7).

Figure 3. Inhibition of IL-4-induced Reporter Activity by IL-4R Neutralizing Antibody in hIL4/IL13 Dual Effector Reporter Cells (Clone 7).

Figure 4. lnhibition of IL-13-induced Reporter Activity by IL-4R Neutralizing Antibody in hIL4/IL13 Dual Effector Reporter Cells.