Title of article :
Interferon-γ Therapy Reduces Blood Leukocyte Levels in Patients with Atopic Dermatitis: Correlation with Clinical Improvement
Author/Authors :
Ellis، نويسنده , , Charles N. and Stevens، نويسنده , , Seth R. and Blok، نويسنده , , Barbara K. and Taylor، نويسنده , , R.Stanley and Cooper، نويسنده , , Kevin D.، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1999
Pages :
7
From page :
49
To page :
55
Abstract :
Atopic dermatitis (AD) is a chronic inflammatory skin disease with abnormalities of both cellular and humoral immunity. Subcutaneous recombinant human interferon-γ (IFN-γ) provides therapeutic benefit to AD patients. In contrast to expectations, IFN-γ does not cause a decrease in the elevated levels of circulating IgE levels in AD patients. We sought to determine cellular targets of IFN-γ treatment that might explain its clinical benefit. Therefore, we evaluated blood leukocyte subsets by multiparameter flow cytometry in AD patients receiving IFN-γ (n = 10) or placebo (n = 11) therapy compared to untreated normal volunteers (n = 14). Treated patients demonstrated reductions in WBC, eosinophil, and lymphocyte counts. Compared to normals, there was a reduced CD4/CD8 ratio in AD patients among activated, large mononuclear cells that was partially corrected with IFN-γ treatment. Clinical improvement correlated with reductions in WBC (r = 0.9, P = 0.0003), eosinophil (r = 0.7, P = 0.035) and lymphocyte (r = 0.8, P = 0.013) counts, and with normalization of the CD4/CD8 ratio among large lymphocytes (r = 0.9, P = 0.04). The data indicate two potential modes of action for INF-γ in AD. One mechanism represents normalization of selected immunologic abnormalities in AD; a second mechanism may be the modest reduction of circulating inflammatory cells. Adequacy of IFN-γ therapy of AD may depend on bringing about these changes.
Keywords :
Leukocytes , Lymphocytes , interferon-? , atopic dermatitis
Journal title :
Clinical Immunology
Serial Year :
1999
Journal title :
Clinical Immunology
Record number :
1848095
Link To Document :
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