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*
Laboratory of Experimental Immunolgy and Departments of
Pathology and
Gastroenterology, University Hospital Gasthuisberg, University of Leuven, Leuven, Belgium
IL-15 shares biological activities but no significant sequence
homology with IL-2. It induces T cell recruitment to sites of
inflammation, T cell proliferation, and cytokine production and rescue
from apoptosis. The aim of this study was to investigate expression of
IL-15 and its effects on proinflammatory cytokine production in
inflammatory bowel disease (IBD). Immunohistochemistry demonstrated
local IL-15 production by macrophages in inflamed mucosa from IBD
patients. Isolated lamina propria mononuclear cells from these patients
but not from controls produced IL-15 when stimulated with LPS or
IFN-
. Moreover, lamina propria T cells (LP-T) from IBD patients were
more responsive to IL-15 as compared with controls, and IL-15 alone
without a primary T cell stimulus induced IFN- and TNF production by
isolated IBD LP-T cells, especially by LP-T cells from patients with
Crohn’s disease. LP-T cells from IBD patients could induce CD40-CD40
ligand (CD40L) interaction-dependent TNF and IL-12 production by
monocytes in a coculture system. This capacity of LP-T cells was
strongly enhanced by preincubation in IL-15 and was the result of
higher CD40L expression after culture in IL-15. These data indicate
that IL-15 is overexpressed in the inflamed mucosa in IBD and that
IL-15 enhances local T cell activation, proliferation, and
proinflammatory cytokine production by both T cells and macrophages,
the latter via a CD40-CD40L interaction-dependent mechanism. Treatment
directed against IL-15 may have therapeutic potential in
IBD.
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