Surface expression of Fc epsilon RI on Langerhans' cells of clinically uninvolved skin is associated with disease activity in atopic dermatitis, allergic asthma, and rhinitis.
BACKGROUND
Fc epsilon RI expressed on the surface of human epidermal Langerhans' cells facilitates uptake of IgE-associated allergens and plays a pivotal role in the pathogenesis of atopic dermatitis. Seminal results from studies investigating Langerhans' cell Fc epsilon RI in skin biopsy sections or epidermal cell suspensions demonstrate the highest receptor expression in lesional skin of patients with active atopic dermatitis.


OBJECTIVE
We sought to investigate and localize Fc epsilon RI expression on Langerhans' cells within a minimally disturbed tissue environment in clinically uninvolved skin and to compare receptor expression between healthy donors and patients with atopic dermatitis or other allergic diseases.


METHODS
Intact epidermal sheets from skin suction blisters, immunofluorescently stained with Langerhans' cell markers and anti-Fc epsilon RI alpha (mAbs 15E5 and 22E7) or anti-IgE, were examined by means of confocal microscopy. Samples incubated with anti-Fc epsilon RI alpha before or after cell fixation-permeabilization were compared to discriminate between cytoplasmic and membrane localization.


RESULTS
Cytoplasmic Fc epsilon RI alpha chain was found in Langerhans' cells from all donors, irrespective of atopic status. Surface Fc epsilon RI-bound IgE was detected in the skin of individuals with active atopic dermatitis and in the skin of those with active asthma or rhinitis. No surface Fc epsilon RI was expressed in the skin of patients with a clinical history of atopic dermatitis, asthma, or rhinitis whose disease was in remission or in the skin of nonatopic individuals.


CONCLUSIONS
In clinically uninvolved skin, Langerhans' cell-surface Fc epsilon RI expression is not only linked to atopic dermatitis but is also generally associated with allergic disease. This supports the concept of a systemic regulatory mechanism associated with active allergic disease, which is further aggravated by local inflammation in atopic skin lesions.
Semper
Amanda E
AE
Division of Infection, Inflammation and Repair, School of Medicine, University of Southampton, United Kingdom.
Heron
Kyle
K
Woollard
Alexander C s
AC
Kochan
Jarema P
JP
Friedmann
Peter S
PS
Church
Martin K
MK
Reischl
Ilona G
IG
D001249:Asthma / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D002462:Cell Membrane / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000473:pathology / Q000503:physiopathology*; D004817:Epidermis / Q000378:metabolism / Q000473:pathology; D005455:Fluorescent Antibody Technique; D006801:Humans; D006967:Hypersensitivity / Q000150:complications*; D007073:Immunoglobulin E / Q000378:metabolism; D007801:Langerhans Cells / Q000378:metabolism*; D017455:Receptors, IgE / Q000378:metabolism*; D012220:Rhinitis / Q000473:pathology / Q000503:physiopathology*; D012867:Skin / Q000378:metabolism* / Q000473:pathology; D013194:Staining and Labeling
D017455:Receptors, IgE; D007073:Immunoglobulin E