Human IL-6 Antibody Summary
Pro29-Met212
Accession # Q75MH2
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
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IL‑6 in Human PBMCs. IL‑6 was detected in immersion fixed human peripheral blood mononuclear cells (PBMCs) treated with PHA (left panel; positive staining) and untreated PBMCs (right panel; negative control) using Mouse Anti-Human IL‑6 Monoclonal Antibody (Catalog # MAB95401) at 8 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (red; NL007) and counterstained with DAPI (blue). Specific staining was localized to cell surface. Staining was performed using our protocol for Fluorescent ICC Staining of Non-adherent Cells.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: IL-6
Interleukin-6 (IL-6) is a pleiotropic, alpha -helical, 22-28 kDa phosphorylated and variably glycosylated cytokine that plays important roles in the acute phase reaction, inflammation, hematopoiesis, bone metabolism, and cancer progression (1-5). Mature human IL-6 is 183 amino acids (aa) in length and shares 39% aa sequence identity with mouse and rat IL-6 (6). Alternative splicing generates several isoforms with internal deletions, some of which exhibit antagonistic properties (7-10). IL-6 induces signaling through a cell surface heterodimeric receptor complex composed of a ligand binding subunit (IL-6 R alpha) and a signal transducing subunit (gp130). IL-6 binds to IL-6 R alpha, triggering IL-6 R alpha association with gp130 and gp130 dimerization (11). gp130 is also a component of the receptors for CLC, CNTF, CT-1, IL-11, IL-27, LIF, and OSM (12). Soluble forms of IL-6 R alpha are generated by both alternative splicing and proteolytic cleavage (5). In a mechanism known as trans-signaling, complexes of soluble IL-6 and IL-6 R alpha elicit responses from gp130-expressing cells that lack cell surface IL-6 R alpha (5). Trans-signaling enables a wider range of cell types to respond to IL-6, as the expression of gp130 is ubiquitous, while that of IL-6 R alpha is predominantly restricted to hepatocytes, monocytes, and resting lymphocytes (2, 5). Soluble splice forms of gp130 block trans-signaling from IL-6/IL-6 R alpha but not from other cytokines that use gp130 as a co-receptor (5, 13). IL-6, along with TNF-alpha and IL-1, drives the acute inflammatory response and the transition from acute inflammation to either acquired immunity or chronic inflammatory disease (1-5). When dysregulated, it contributes to chronic inflammation in obesity, insulin resistance, inflammatory bowel disease, arthritis, sepsis, and atherosclerosis (1, 2, 5). IL-6 can also function as an anti-inflammatory molecule, as in skeletal muscle where it is secreted in response to exercise (2). In addition, it enhances hematopoietic stem cell proliferation and the differentiation of Th17 cells, memory B cells, and plasma cells (1, 14).
- Mansell, A. and B.J. Jenkins (2013) Cytokine Growth Factor Rev. 24:249.
- Schuett, H. et al. (2009) Thromb. Haemost. 102:215.
- Erta, M. et al. (2012) Int. J. Biol. Sci. 8:1254.
- Garbers, C. et al. (2012) Cytokine Growth Factor Rev. 23:85.
- Mihara, M. et al. (2012) Clin. Sci. (Lond.) 122:143.
- Hirano, T. et al. (1986) Nature 324:73.
- Kestler, D.P. et al. (1995) Blood 86:4559.
- Kestler, D.P. et al. (1999) Am. J. Hematol. 61:169.
- Bihl, M.P. et al. (2002) Am. J. Respir. Cell Mol. Biol. 27:48.
- Alberti, L. et al. (2005) Cancer Res. 65:2.
- Murakami, M. et al. (1993) Science 260:1808.
- Muller-Newen, G. (2003) Sci. STKE 2003:PE40.
- Mitsuyama, K. et al. (2006) Clin. Exp. Immunol. 143:125.
- Cerutti, A. et al. (1998) J. Immunol. 160:2145.
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