Immunologic reactions are customarily divided into two broad categorie
s, cell-mediated and antibody-mediated. An interplay between these two
pathogenetic principles is indicated by reactions such as cutaneous b
asophil hypersensitivity, late-phase reaction, and cutaneous lesions i
ndistinguishable from regular allergic contact dermatitis lesions afte
r sensitization with IgE antibodies against certain haptens. In the pr
esent study, 23 patients with a history of a positive epicutaneous tes
t to formaldehyde participated. On retest, 15 showed a positive reacti
on. Eight patients were Phadiatop(R) positive, indicating an atopic di
athesis, and eight had a history of or ongoing atopic dermatitis. On R
AST test(R), only two, nonatopic patients had specific IgE antibodies
to formaldehyde. In the cellular infiltrates of biopsies from epicutan
eous test sites, cells reactive with monoclonal antibodies against IgE
were found in positive and negative formalin tests, both in atopics a
nd nonatopics, as well as in control biopsies from nonlesional skin. D
ouble immunofluorescence staining experiments showed that IgE occurred
on Langerhans' cells. The proportion of IgE-positive cells correlated
to the level of serum IgE, but not to atopy. These cells were also fo
und both in the epidermis and in the dermis in nonatopic patients. ICA
M-1 occurred on keratinocytes in all patient groups. This study does n
ot support the hypothesis that specific IgE antibodies are active in t
he pathogenesis of contact sensitivity to formaldehyde either in atopi
c or in nonatopic patients.