Effects of interferon-alpha-2b on the clinical course, inflammatory skin infiltrates and peripheral blood lymphocytes in patients with severe atopic eczema.
Increased serum IgE and enhanced susceptibility to viral infections, decreased levels of interferons, lymphocytic skin infiltrates and IgE-bearing epidermal Langerhans cells are striking features in patients with atopic eczema (AE). Since the hyper-IgE syndrome is known to improve under alpha-interferon (alpha-IFN) therapy, we treated 7 patients with severe AE and high serum IgE exclusively with 3 x 10(6) units IFN alpha 2b thrice weekly for 3 months. Before treatment the skin infiltrates mainly consisted of CD3+/CD4+/TcR alpha/beta + lymphocytes, whereas the CD3+/CD8+ phenotype was limited to about 10% of cells. After 6 weeks of therapy, epidermal inflammation with CD4+ and CD8+ cells was reduced but dense infiltrates remained in papillary perivascular areas. Expression of TcR gamma/delta, HLA-DR and CD25 showed no significant changes. Initially high serum IgE and soluble CD23 as well as cell-bound IgE dropped under therapy, whereas a short-term elevation in serum IL-2 receptor was observed. On peripheral blood lymphocytes slightly reduced expression of HLA-DR, LFA-1, CD23 and ICAM-1 was seen after 100 days. LFA-3 expression became reduced in 4 patients, the CD4/CD8 ratio decreased in all cases. After an initial therapeutic response of all patients, significant longer-lasting improvement of the skin lesions could only be observed in 2 of 7 patients. The data of our long-term study suggest that systemic IFN alpha 2b treatment leads to a remarkable reduction in epidermal inflammation but does not significantly influence cutaneous cell subsets. Immunomodulatory effects became obvious by reduced peripheral cell subsets expressing TcR alpha/beta, MHC class II and adhesion molecules.
Gruschwitz
M S
MS
Department of Dermatology, University of Erlangen-Nuremberg Medical School, FRG.
Peters
K P
KP
Heese
A
A
Stosiek
N
N
Koch
H U
HU
Hornstein
O P
OP
D000328:Adult; D003876:Dermatitis, Atopic / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D005260:Female; D006801:Humans; D007106:Immune Sera / Q000032:analysis; D007073:Immunoglobulin E / Q000097:blood; D016130:Immunophenotyping; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000276:immunology / Q000627:therapeutic use*; D015847:Interleukin-4 / Q000097:blood; D007958:Leukocyte Count / Q000187:drug effects; D016131:Lymphocyte Subsets / Q000187:drug effects*; D008297:Male; D017455:Receptors, IgE / Q000187:drug effects; D015375:Receptors, Interleukin-2 / Q000187:drug effects; D011994:Recombinant Proteins; D012867:Skin / Q000276:immunology / Q000473:pathology*
D007106:Immune Sera; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D017455:Receptors, IgE; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins; D015847:Interleukin-4; D007073:Immunoglobulin E