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Journal of Asthma, Allergy and Clinical Immunology ; : 912-919, 1999.
Article in Korean | WPRIM | ID: wpr-158721

ABSTRACT

BACKGROUND: Monocytes and T helper cells play major roles in the immunologic dysfunction of atopic dermatitis (AD). Many studies have been done on the cytokine pattern to evaluate abnormalities or differences of immune cells in AD, but the results were conflicting among studies and most of these previous reports were performed with various kinds of mitogen-stimulation. OBJECTIVE: The purpose of this study was to investigate spontaneous cytokine pattern in peripheral blood mononuclear cells (PBMC) from patients with AD. We focused on the expression of monokines that had effects on monocytes and T cells. METHODS: We measured mRNA expression of IL-10, GM-CSF and TNF-alpha in freshly isolated PBMC with semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR). The intensity of cytokine cDNA was normalized to that of beta-actin product as a standard marker. RESULTS: IL-10 mRNA expression was significantly enhanced in AD compared:with control subjects (p<0.05). Spontaneous mRNA expression of TNF-alpha was significantly lower in AD patients (p <0.01). The level of GM-CSF mRNA expression was heterogeneous and spontaneous mRNA expression was slightly increased in AD although the difference did not reach the level of statistical significance. CONCLUSION: Our data was able to represent in vivo cytokine expression state of PBMC in atopic dermatitis. Increased expression of IL-10 and GM-CSF may have been associated with monocyte dysfunction in AD although increase in the expression of GM-CSF mRNA was not statistically significant. TNF-alpha mRNA expression was decreased in AD and increased IL-10 was suggested to exert an inhibitory effect on the expression of TNF-alpha mRNA.


Subject(s)
Humans , Actins , Dermatitis, Atopic , DNA, Complementary , Granulocyte-Macrophage Colony-Stimulating Factor , Interleukin-10 , Monocytes , Monokines , RNA, Messenger , T-Lymphocytes , T-Lymphocytes, Helper-Inducer , Tumor Necrosis Factor-alpha
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