Human IL-16 ELISA Kit

INTENDED USE

This Human Interleukin-16 (IL-16) ELISA Kit is to be used for the in vitro quantitative determination of human IL-16 concentrations in serum, plasma, cell culture supernatant, and other biological fluids. This kit is intended FOR LABORATORY RESEARCH PURPOSES ONLY and is not for use in diagnostic or therapeutic procedures.

INTRODUCTION

Interleukin-16 (IL-16) discovered in 1982¹, known formerly as lymphocyte chemoattractant factor (LCF) is a lymphocyte chemoattractant factor of T cell origin with selective activity for CD4⁺ T cells.  LCF was designated interleukin-16 (IL-16) in 1995.  IL-16 is a product of CD8⁺ cells, CD4⁺ cells², eosinophils³, mast cells and epithelial cells derived from asthmatics⁴.  Expression of IL-16 in asthmatic epithelium correlates with the number of infiltrating CD4⁺ T cells⁵. 

LCF was originally identified and purified from the supernatants of ConA-stimulated peripheral blood mononuclear cells (PBMC).  In addition to its chemotactic activity, it is a competence growth factor selective for CD4⁺ T cells dependent on an interaction with CD4 for induction of functional activity.  Its cDNA codes for a novel 14-kDa protein into a homotetrameric form is required for induction of biologic activity.  IL-16 appears in culture supernatants as a relative molecular mass (Mr) ~56,000 biologically active, non-covalently linked tetramer, but migrates in monomeric form in SDS PAGE.  Eluted monomeric peptides are inactive but reaggregate to Mr 56,000 regaining biological activity⁶.  The protein expressed from the IL-16 cDNA demonstrates all the functions and chemical features of the native protein, including an identical pI, and autoaggregation into functional tetramers.

IL-16 is performed and stored in biologically active form in CD8⁺. T cells from which it is secreted following stimulation with histamine via H2 type receptors.  The secretory process occurs within 4 hrs and does not require transcription, translation, or new protein synthesis.

IL-16’s ability to inhibit the MLR and other antigen induced activation suggests that it may be useful in inhibiting allograft rejection.  Because IL-16 selectively induces IL-2 responsiveness in CD4⁺ T cells it may be useful (along with IL-2) for selective CD4⁺ T cell immune reconstitution in individuals with lymphopenia, for example following chemotherapy or HIV-1 infection.  In the latter circumstance, its ability to inhibit HIV transcription should provide a protective role if used as a therapy in HIV-1 infected individuals⁷. 

Inhibitors of IL-16 chemotactic function may be useful in diseases in which it appears to play a prominent role in the inflammatory process.  The presence of IL-16 early after antigen challenge in asthma⁸, the marked upregulation of IL-16 synthesis by epithelium of asthmatics along with the correlation of IL-16 protein with the number of infiltrating CD4⁺ T cells in the airways of human asthmatics suggest that therapeutics aims at blocking IL-16 synthesis or function may be valuable in this disease.

This IL-16 ELISA is a 4.5 hour solid phase immunoassay readily applicable to measure IL-16 in serum, plasma, cell culture supernatant, and other biological fluids in the range of 0 to 3200 pg/mL.  It showed no cross-reactivity with other cytokines tested such as EGF, EPO, GM-CSF, IL-1β, IL-7, IL-8, IFN-γ, MCAF, MCP-3, M-CSF, SAA, TGF-β, and TNF-α.