IFN-gamma plays a dominant role in upregulation of Candida-specific IgE synthesis in patients with atopic dermatitis.
BACKGROUND
Although Candida albicans (CA) is known to induce Th1 clones that suppress IgE synthesis, serum IgE antibody against CA is often increased in atopic patients. This study aims to elucidate the mechanism of IgE synthesis against CA in atopic patients.


METHODS
We measured the production of IL-4 and IFN-gamma by peripheral blood mononuclear cells (PBMCs) from atopic patients upon stimulation with CA and examined the correlation with the level of serum IgE antibody against CA.


RESULTS
The level of serum CA-specific IgE antibody (CA-IgE) was significantly higher in patients with atopic dermatitis (AD) than in patients with bronchial asthma (BA) (geometric mean = 3.6 vs. 0.27 U(A)/ml, p < 0.02) (U(A) = unit allergen), while there was no difference in the level of house dust mite-specific IgE antibody between them (67.6 vs. 87.1 U(A)/ml). Although IL-4 production by PBMCs upon stimulation with CA in patients with AD was not significantly different from that in patients with BA (mean = 359.1 vs. 515.3 fg/ml), IFN-gamma production was significantly lower in the former than in the latter group (8.1 vs. 56.2 pg/ml, p < 0.001). Consequently, the ratio of IL-4/IFN-gamma production was apparently higher in patients with AD than in those with BA, which corresponds to the difference between them in the level of serum CA-IgE. A significant negative correlation was seen in patients with AD between IFN-gamma production by CA-stimulated PBMCs and the level of serum CA-IgE (p < 0.05).


CONCLUSIONS
IgE synthesis against CA in atopic patients may be precipitated not by enhancing IL-4 production, but by reducing IFN-gamma secretion.
Kimura
M
M
Department of Allergy and Clinical Immunology, Shizuoka Children's Hospital, Shizuoka, Japan.
Tsuruta
S
S
Yoshida
T
T
D000293:Adolescent; D000908:Antibodies, Fungal / Q000096:biosynthesis; D002175:Candida / Q000276:immunology*; D002648:Child; D002675:Child, Preschool; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000382:microbiology; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007371:Interferon-gamma / Q000096:biosynthesis / Q000502:physiology*; D015847:Interleukin-4 / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D008297:Male; D015854:Up-Regulation
D000908:Antibodies, Fungal; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma