Immunology
Publisher
Springer London
Reference17 articles.
1. Spergel JM. From atopic dermatitis to asthma: the atopic march. Ann Allergy Asthma Immunol. 2010;105(2):99–106. This article discusses the pathogenetic etiology of the “atopic march,” a phenomenon describing the sequential development of atopic dermatitis, asthma, and allergic rhinitis in children. The author was particularly interested in how asthma and allergic rhinitis ensue from atopic dermatitis, which is a manifestation of dysfunctional barrier function of the epidermis. He discusses supporting evidence in the literature for environmental, immunologic, and genetic predisposing factors in susceptible individuals, including loss-of-function mutations in the filaggrin gene.
2. Walsh GA, Richards KL, Douglas SD, Blumenthal MN. Immunoglobulin E anti-Staphylococcus aureus antibodies in atopic patients. J Clin Microbiol. 1981;13(6):1046–8. The authors used a solid-phase radioallergoabsorbent assay to demonstrate increased IgE binding to S. aureus in patients with eczema.
3. Tokura Y. Extrinsic and intrinsic types of atopic dermatitis. J Dermatol Sci. 2010;58(1):1–7. A review of IgE-associated extrinsic atopic dermatitis and non-IgE-associated intrinsic atopic dermatitis, discussing the immunologic state of both conditions including chemokines, cytokines, immunoglobulins, and B and T cells of adaptive immunity.
4. De Benedetto A, Agnihothri R, McGirt LY, Bankova LG, Beck LA. Atopic dermatitis: a disease caused by innate immune defects? J Invest Dermatol. 2009;129(1):14–30. A thorough review of atopic dermatitis and the contribution of the complex interplay of the innate immune system to its pathogenesis. This includes activation of the TLR2 receptors, disruption of the epithelial barrier, and the role of the adaptive immune system.
5. Allen HB, Mueller JL. A novel finding in atopic dermatitis: film-producing Staphylococcus epidermidis as an etiology. Int J Dermatol. 2011;50(8):992–3. Atopic dermatitis is also known as the “itch that rashes.” In this paper we addressed the question of what causes the itch by providing evidence that atopic dermatitis is subclinical miliaria. We discovered biofilm and Staphylococcus epidermidis—but no Staphylococcus aureus—in skin scrapings from a patient with flexural eczema. Based on what is known about biofilm-producing S. epidermidis and miliaria, we hypothesized that subsequent blockage of eccrine sweat ducts, as was initially demonstrated by Sulzberger et al. in eczema, leads to intense pruritus, which when scratched leads to damage to an already compromised filaggrin-deficient stratum corneum and the well-known chronic inflammatory state of eczema.