Anna R Smith1, George Knaysi2,3, Jeffrey M Wilson1, Julia A Wisniewski4,5. 1. Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, 22908, USA. 2. Department of Public Health Sciences, University of Virginia School of Medicine, Charlottesville, VA, 22908, USA. 3. Geisel School of Medicine, Dartmouth College, 1 Rope Ferry Road, Hanover, NH, 03755, USA. 4. Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, 22908, USA. jaw4he@virginia.edu. 5. Department of Pediatrics, University of Virginia School of Medicine, Charlottesville, VA, 22908, USA. jaw4he@virginia.edu.
Abstract
PURPOSE OF REVIEW: To highlight recent contributions in the literature that enhance our understanding of the cutaneous immune response to allergen. RECENT FINDINGS: Defects in skin barrier function in infancy set the stage for the development of atopic dermatitis (AD) and allergy. Both genetic and environmental factors can contribute to damage of the stratum corneum (SC), with activation of specific protease enzymes under high pH conditions playing a key role. Immune cells and mediators in the dermis and epidermis impair SC repair mechanisms and support allergy development. In barrier-disrupted skin, type 2 innate lymphoid cells (ILC2s), mast cells (MCs), and basophils have been shown to promote AD and pathogenic Th2 responses in murine models. Skin barrier disruption favors induction of systemic Th2-associated inflammatory pathways. A better understanding of the ontogeny and regulation of these complex networks in infant skin is needed to guide future strategies for allergy treatment and prevention.
PURPOSE OF REVIEW: To highlight recent contributions in the literature that enhance our understanding of the cutaneous immune response to allergen. RECENT FINDINGS: Defects in skin barrier function in infancy set the stage for the development of atopic dermatitis (AD) and allergy. Both genetic and environmental factors can contribute to damage of the stratum corneum (SC), with activation of specific protease enzymes under high pH conditions playing a key role. Immune cells and mediators in the dermis and epidermis impair SC repair mechanisms and support allergy development. In barrier-disrupted skin, type 2 innate lymphoid cells (ILC2s), mast cells (MCs), and basophils have been shown to promote AD and pathogenic Th2 responses in murine models. Skin barrier disruption favors induction of systemic Th2-associated inflammatory pathways. A better understanding of the ontogeny and regulation of these complex networks in infant skin is needed to guide future strategies for allergy treatment and prevention.
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