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Division of Allergy and Immunology, Department of Pediatrics, The National Jewish Medical and Research Center, Denver, CO 80206;
Meakins-Christie Laboratories, McGill University, Montréal, Québec, Canada;
Departments of Dermatology and Pharmacology, Indiana University Medical Center, Indianapolis, IN 46202; and
Department of Pediatrics, University of Colorado Health Sciences Center, Denver, CO 80262
PBMC and acute skin lesions of patients with atopic dermatitis (AD)
are characterized by increased IL-4 and IL-13, but decreased IFN-
production. This bias toward an increased Th2 cytokine profile may
contribute to the elevated IgE levels and acute skin inflammation seen
in AD. In this study, we examined the levels of IL-15, a Th1-like
cytokine, in the PBMC and the skin lesions of AD patients. IL-15
secretion by Staphylococcal enterotoxin B-treated PBMC of AD patients
was significantly lower than that of normals and psoriasis patients
(p < 0.001). Membrane-bound IL-15 expression as
measured by mean fluorescence intensity and percentage of
IL-15-positive cells in Staphylococcal enterotoxin B-treated monocytes
of AD patients (644 ± 49% and 12.7 ± 0.6%, respectively)
were significantly lower than that of normals (869 ± 56% and
15.8 ± 1.2%, respectively) and psoriasis patients (1488 ±
217% and 22.7 ± 0.8%, respectively; p <
0.0007 and p < 0.0001, respectively). The
membrane-bound IL-15 expression was also significantly lower in the
control monocytes of AD patients compared with that in normals and
psoriasis patients. There was no significant difference in the absolute
number or percentage of monocytes between the study subjects. However,
psoriasis skin lesions were found to have significantly more IL-15
mRNA-expressing cells (22.4 ± 1.7) compared with that in acute AD
(7.5 ± 1.7) and chronic AD (13.7 ± 1.7) skin lesions
(p < 0.05). IL-15 enhanced IFN- production by
the PBMC of AD patients (p < 0.01), but not by
that of normal individuals or psoriasis patients. In addition, IL-15
was found to suppress IgE synthesis (p < 0.01) by
the PBMC of AD patients. These data support the concept that reduced
IL-15 expression may contribute to the pathogenesis of
AD.
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