|Detection of IL‑13 in Human PBMCs by Flow Cytometry. Human peripheral blood mononuclear cells (PBMCs) treated with 5 ng/mL Recombinant Human IL‑4 (Catalog # 204-IL) and 10 µg/mL Goat Anti-Human IFN‑ gamma Antigen Affinity-purified Polyclonal Antibody (Catalog # AF-285-NA) for 3 days were stained with Mouse Anti-Human IL‑13 Monoclonal Antibody (Catalog # MAB2131) followed by Allophycocyanin-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # F0101B) and Mouse Anti-Human CD4 PE-conjugated Monoclonal Antibody (Catalog # FAB3791P). Quadrant markers were set based on control antibody staining (Catalog # MAB002).|
Cell Proliferation Induced by IL‑13 and Neutralization by Human IL‑13 Antibody. Recombinant Human IL‑13 (Catalog # 213-ILB) stimulates proliferation in the TF‑1 human erythroleukemic cell line in a dose-dependent manner (orange line). Proliferation elicited by Recombinant Human IL‑13 (10 ng/mL) is neutralized (green line) by increasing concentrations of Mouse Anti-Human|
IL‑13 Monoclonal Antibody (Catalog # MAB2131). The ND50 is typically 1-4 µg/mL.
IL-13 is a 17 kDa immunoregulatory cytokine that plays a key role in the pathogenesis of allergic asthma and atopy. It is secreted by Th1 and Th2 CD4+ T cells, NK cells, visceral smooth muscle cells, eosinophils, mast cells, and basophils (1-3). IL-13 circulates as a monomer with two internal disulfide bonds that contribute to a bundled four alpha -helix configuration (4, 5). Mature human IL-13 shares 57%, 59%, and 94% amino acid sequence identity with mouse, rat, and rhesus IL-13, respectively. Despite the low homology, it exhibits cross-species activity between human, mouse, and rat (6, 7). IL-13 has diverse activities on numerous cell types (8). On macrophages, IL-13 suppresses the production of proinflammatory cytokines and other cytotoxic substances. On B cells, IL-13 induces immunoglobulin class switching to IgE, upregulates the expression of MHC class II, CD71, CD72, and CD23, and costimulates proliferation. IL-13 upregulates IL-6 while downregulating IL-1 and TNF-alpha production by fibroblasts and endothelial cells. IL-13 binds with low affinity to IL-13 R alpha 1, triggering IL-13 R alpha 1 association with IL-4 R alpha. This high affinity receptor complex also functions as the type 2 IL-4 receptor complex (9, 10). Additionally, IL-13 binds with high affinity to IL-13 R alpha 2 which is expressed intracellularly, on the cell surface, and as a soluble molecule (11-14). IL-13 R alpha 2 regulates the bioavailability of both IL-13 and IL-4 and is over-expressed in glioma and several bronchial pathologies (10, 15, 16). Compared to wild type IL-13, the atopy-associated R110Q variant of IL-13 elicits increased responsiveness from eosinophils that express low levels of IL-13 R alpha 2 (17).
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