Human IL-32 Alexa Fluor® 594-conjugated Antibody

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.

Preparation and Storage

Background: IL-32

Interleukin 32 (IL-32) is an N-glycosylated cytokine that is upregulated by inflammatory stimulation in monocytes, NK cells, epithelial cells, and pancreatic myofibroblasts (1-5). It cooperates with these stimuli to promote the expression of other proinflammatory molecules such as TNF-alpha, IL-6, IL-1 beta, IL-1 alpha, and CXCL8/IL‑8 (5-7). The longest of several IL-32 splicing variants is the 20-25 kDa gamma isoform which is also known as natural killer cell transcript 4 (NK4) (8, 9). The alpha isoform (IL-32 alpha ) lacks a portion of the putative signal peptide as well as 57 aa from the C-terminal region. IL-32 alpha is less potent than IL-32 beta, gamma, or δ at inducing the expression of proinflammatory molecules in peripheral blood mononuclear cells (PBMC) (8, 10). Neutrophil-derived Proteinase 3 (PR3) cleaves IL-32 alpha between Thr57 and Val58, a cleavage site that is retained in other IL-32 isoforms (11). The N-terminal fragment of PR3-cleaved IL-32 alpha shows increased potency at inducing CXCL2/MIP-2 and CXCL8 expression in PBMC relative to uncleaved IL-32 alpha (11, 12). IL-32 is highly expressed by colonic epithelial cells in inflammatory bowel disease and Crohn’s disease, rheumatoid arthritis synovium, and ductal epithelial cells in chronic pancreatitis and pancreatic cancer (5, 13-15). IL-32 inhibits HIV-1 replication in vitro, and it is elevated in the serum of HIV-1 patients (16, 17).

Product Datasheets

Related Research Areas

• Cytokines and Receptors in Allergy and Asthma
• Inflammatory Mediators
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• T Cell Cytokine Signaling