Absence of specific IgE antibodies in allergic contact sensitivity to formaldehyde

Abstract

Immunologic reactions are customarily divided into two broad categories, cell-mediated and antibody-mediated. An interplay between these two pathogenetic principles is indicated by reactions such as cutaneous basophil hypersensitivity, late-phase reaction, and cutaneous lesions indistinguishable from regular allergic contact dermatitis lesions after sensitization with IgE antibodies against certain haptens. In the present study, 23 patients with a history of a positive epicutaneous test to formaldehyde participated. On retest, 15 showed a positive reaction. Eight patients were Phadiatop positive, indicating an atopic diathesis, and eight had a history of or ongoing atopic dermatitis. On RAST test, only two, nonatopic patients had specific IgE antibodies to formaldehyde. In the cellular infiltrates of biopsies from epicutaneous test sites, cells reactive with monoclonal antibodies against IgE were found in positive and negative formalin tests, both in atopics and nonatopics, as well as in control biopsies from nonlesional skin. Double 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 found both in the epidermis and in the dermis in nonatopic patients. ICAM-1 occurred on keratinocytes in all patient groups. This study does not support the hypothesis that specific IgE antibodies are active in the pathogenesis of contact sensitivity to formaldehyde either in atopic or in nonatopic patients.

Comparison of cytokine secretion profiles provoked in mice by glutaraldehyde and formaldehyde

“…An important consideration is the fact that in the experiments described here, a differential quality of immune response is induced following cutaneous exposure to formaldehyde or glutaraldehyde. As such, the preferential activation of type 1, IFN‐γ‐secreting, LNCs and the failure to elicit increases in the total serum concentration of IgE following topical application of formaldehyde to mice [ 38, 41], are consistent with the inability to detect specific IgE antibody in patients with formaldehyde‐induced atopic dermatitis [ 45]. There is good reason to suppose that, due to the systemic nature of the immune system, topical exposure to chemical respiratory allergens can result in effective sensitization of the respiratory tract.…”

Role of Transient Receptor Potential Ion Channels and Evoked Levels of Neuropeptides in a Formaldehyde-Induced Model of Asthma in Balb/c Mice

“…Several epidemiological studies have demonstrated that FA exposure can induce or exacerbate asthma [34]–[37]. Unlike typical allergens, FA-specific IgE is rarely detected [38], [39], which suggests that FA may be involved in asthma via a non-IgE-mediated mechanism. Two possible pathways for FA-induced asthma have been proposed: the irritant effect and the adjuvant effect [40].…”

Relationship between Exposure to Formaldehyde and Immunoglobulin E (IgE) Production during the Gross Anatomy Laboratory

“…Dykewicz et al 13) suggested that clinical IgE-mediated allergy to gaseous FA does not exist, or if it does, is extremely rare. Also, a study by Liden et al 14) did not support the hypothesis that specific IgE antibodies are active in the pathogenesis of contact sensitivity to FA either in atopic or nonatopic patients. Thus IgE-mediated sensitization to FA is controversial, as mentioned above.…”