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This month's theme
Contents
T HE J OURNAL OF
Allergy Clinical Immunology AND
VOLUME 118 NUMBER 1 d
OFFICIAL JOURNAL OF THE AMERICAN ACADEMY OF ALLERGY, ASTHMA AND IMMUNOLOGY
Y
This month’s theme: Atopic dermatitis About the cover
The Journal’s July cover highlights 2 phases of atopic dermatitis (AD) that arise from the complex interaction of genetic and environmental factors. The depiction of the first phase captures the cutaneous hyperreactivity of nonlesional skin resulting from a genetically predisposed, defective skin barrier that allows the penetration of allergens and microbial infection. This results in a ‘‘primed’’ skin immune response poised to overreact to environmental stimuli. This priming response is facilitated by IgE-armed Langerhans cells and mast cells, as well as the chronic infiltration of skin homing TH2 memory T cells. In the second phase of AD, the acute skin infiltrate develops as the result of a complex immune response driven by the release of proinflammatory cytokines and chemokines from multiple resident cell types, including keratinocytes, endothelial cells, Langerhans cells, and monocytes/macrophages. (Abbreviations: CCL, Chemokine [C-C motif] ligand; CCR, chemokine receptor; CLA, cutaneous lymphocyteassociated antigen; EOS, eosinophil; HBD, human b defensin; LC, Langerhans cell; MC, mast cell; MO, monocyte; PMN, polymorphonucleocyte; SCCE, stratum corneum chymotryptic enzyme; SCTE, stratum corneum tryptic enzyme; TSLP, human thymic stromal lymphopoietin.) This month’s feature issue on AD offers an excellent review of our current knowledge of genetics, skin barrier function, and immunology of AD as discussed in outstanding articles by Cork et al, Morar et al, Homey et al, McGirt and Beck, and others. Additionally the EAACI/AAAAI/PRACTALL consensus report on AD, the Clinical Pearls feature by Boguniewicz et al, and the Images in Allergy atlas by Fiset et al offer the reader an understanding of the pathophysiology of AD, which holds importance for therapeutic and management issues associated with this disease. Articles relevant to the AD theme are noted in the Table of Contents by a red starburst beside their titles. Cover design by JDI, LLC under the guidance of Drs Donald Leung, Bernhard Homey, Lisa Beck, and Natalija Novak. This month in Beyond Our Pages A large epidemiologic study addressed the important subject of the effects of the timing of solid food introduction in infancy on the subsequent occurrence of atopic dermatitis and allergic sensitization. d Exciting new findings point to a likely genetic basis for eosinophilic esophagitis. d Findings up to 2 years after bronchial thermoplasty, a provocative new approach to asthma treatment, have been described. d The role of T cells in asthma might be redefined by the discovery of an increased frequency of natural killer T cells in the lungs of asthmatic patients. d Experimental asthma can be blocked by interfering with certain costimulatory signals in T-cell activation. d Genetic variants of filaggrin, a protein involved in the formation of a normal skin barrier, might predispose to the occurrence of eczematous states, including atopic dermatitis. Ó 2006 American Academy of Allergy, Asthma and Immunology The Journal of Allergy and Clinical Immunology (ISSN: 0091-6749) is published monthly by Elsevier Inc., 360 Park Avenue South, New York, NY 100101710. Business Office: 1600 John F. Kennedy Boulevard, Suite 1800, Philadelphia, PA 19103-2899. Editorial Office: 11830 Westline Industrial Drive, St Louis, MO 63146-3318. Customer Service Office: 6277 Sea Harbor Drive, Orlando, FL 32887-4800. Periodicals postage paid at New York, NY and additional mailing offices. POSTMASTER: Send address changes to The Journal of Allergy and Clinical Immunology, Elsevier Periodicals Customer Service, 6277 Sea Harbor Drive, Orlando, FL 32887-4800.
J ALLERGY CLIN IMMUNOL
July 2006 5A
T HE J OURNAL OF
Allergy Clinical Immunology AND
VOLUME 118 NUMBER 1 d
OFFICIAL JOURNAL OF THE AMERICAN ACADEMY OF ALLERGY, ASTHMA AND IMMUNOLOGY
Y
This month’s theme: Atopic dermatitis About the cover
The Journal’s July cover highlights 2 phases of atopic dermatitis (AD) that arise from the complex interaction of genetic and environmental factors. The depiction of the first phase captures the cutaneous hyperreactivity of nonlesional skin resulting from a genetically predisposed, defective skin barrier that allows the penetration of allergens and microbial infection. This results in a ‘‘primed’’ skin immune response poised to overreact to environmental stimuli. This priming response is facilitated by IgE-armed Langerhans cells and mast cells, as well as the chronic infiltration of skin homing TH2 memory T cells. In the second phase of AD, the acute skin infiltrate develops as the result of a complex immune response driven by the release of proinflammatory cytokines and chemokines from multiple resident cell types, including keratinocytes, endothelial cells, Langerhans cells, and monocytes/macrophages. (Abbreviations: CCL, Chemokine [C-C motif] ligand; CCR, chemokine receptor; CLA, cutaneous lymphocyteassociated antigen; EOS, eosinophil; HBD, human b defensin; LC, Langerhans cell; MC, mast cell; MO, monocyte; PMN, polymorphonucleocyte; SCCE, stratum corneum chymotryptic enzyme; SCTE, stratum corneum tryptic enzyme; TSLP, human thymic stromal lymphopoietin.) This month’s feature issue on AD offers an excellent review of our current knowledge of genetics, skin barrier function, and immunology of AD as discussed in outstanding articles by Cork et al, Morar et al, Homey et al, McGirt and Beck, and others. Additionally the EAACI/AAAAI/PRACTALL consensus report on AD, the Clinical Pearls feature by Boguniewicz et al, and the Images in Allergy atlas by Fiset et al offer the reader an understanding of the pathophysiology of AD, which holds importance for therapeutic and management issues associated with this disease. Articles relevant to the AD theme are noted in the Table of Contents by a red starburst beside their titles. Cover design by JDI, LLC under the guidance of Drs Donald Leung, Bernhard Homey, Lisa Beck, and Natalija Novak. This month in Beyond Our Pages A large epidemiologic study addressed the important subject of the effects of the timing of solid food introduction in infancy on the subsequent occurrence of atopic dermatitis and allergic sensitization. d Exciting new findings point to a likely genetic basis for eosinophilic esophagitis. d Findings up to 2 years after bronchial thermoplasty, a provocative new approach to asthma treatment, have been described. d The role of T cells in asthma might be redefined by the discovery of an increased frequency of natural killer T cells in the lungs of asthmatic patients. d Experimental asthma can be blocked by interfering with certain costimulatory signals in T-cell activation. d Genetic variants of filaggrin, a protein involved in the formation of a normal skin barrier, might predispose to the occurrence of eczematous states, including atopic dermatitis. Ó 2006 American Academy of Allergy, Asthma and Immunology The Journal of Allergy and Clinical Immunology (ISSN: 0091-6749) is published monthly by Elsevier Inc., 360 Park Avenue South, New York, NY 100101710. Business Office: 1600 John F. Kennedy Boulevard, Suite 1800, Philadelphia, PA 19103-2899. Editorial Office: 11830 Westline Industrial Drive, St Louis, MO 63146-3318. Customer Service Office: 6277 Sea Harbor Drive, Orlando, FL 32887-4800. Periodicals postage paid at New York, NY and additional mailing offices. POSTMASTER: Send address changes to The Journal of Allergy and Clinical Immunology, Elsevier Periodicals Customer Service, 6277 Sea Harbor Drive, Orlando, FL 32887-4800.
J ALLERGY CLIN IMMUNOL
July 2006 5A