Commentary
See article on page 795Monocytes or T cells in Crohn's disease: does IL-16 allow both to play at that game?
| The first 150 words of the full text of this article appear below. |
Interleukin (IL)-16 was first described in 1982 under the name "lymphocyte chemoattractant factor".1 Since its cloning in 1994,2 the complex structure and biological function of this cytokine has been extensively explored. In 1999, the IL-16 gene was localised to chromosome 15q26.33 but the role of genetic variants of this gene have yet to be explored in human disease.
IL-16 can be produced by a variety of inflammatory cells, including mast cells, eosinophils, mononuclear phagocytes, and CD4+ and CD8+ T cells.4 IL-16 is expressed as an 80 kDa precursor molecule,5 which is processed to active IL-16 by caspase 3.6
Most interestingly, the main receptor for IL-16 appears to be the CD4
molecule (which identifies T helper cells but is also present on
monocytes and other phagocytes). It is assumed that interaction with
the CD4 molecule is the main event in induction of most IL-16 mediated
biological effects although other receptors and co-receptors may exist.
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