Mechanical Injury Polarizes Skin Dendritic Cells to Elicit a Th2 Response by Inducing Cutaneous TSLP Expression

Oyoshi, Michiko K.; Larson, Ryan; Ziegler, Steven F.; Geha, Raif S.

doi:10.1016/j.jaci.2010.12.1031

Cited by 6 publications

(7 citation statements)

References 16 publications

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“…Th2-mediated differentiation [11,22], rather than tolerance. A review by Larraneta et al [23] on transdermal devices highlights the importance of reducing local erythema, particularly for repetitive treatments (such as AIT) to maintain patient compliance.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

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A low inflammatory, Langerhans cell-targeted microprojection patch to deliver ovalbumin to the epidermis of mouse skin

Burg

Depelsenaire

Crichton

et al. 2019

Journal of Controlled Release

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Section: Accepted Manuscriptmentioning

confidence: 99%

“…Treg) [68,69] or immune activation (e.g. Th1/Th2) [22,70], however, the inflammatory threshold for LC-induced immune activation is yet to be determined. The eMPA defined here induces less skin inflammation than the dMPA, primarily penetrating into the epidermis, resulting in strata-specific APC migration ( Figure 7).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

A low inflammatory, Langerhans cell-targeted microprojection patch to deliver ovalbumin to the epidermis of mouse skin

Burg

Depelsenaire

Crichton

et al. 2019

Journal of Controlled Release

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“…Local mechanical injury in atopic dermatitis leads to the "itch-scratch" cycle in patients with atopic dermatitis and perpetuates disease activity (Boguniewicz and Leung, 2010). To induce mechanical injury, we performed tape stripping on mouse ears followed by epicutaneous application with soluble antigen in IgE-sensitized mice, in a manner akin to published protocols (Oyoshi et al, 2010). After tape stripping and antigen application, the absence of basophils significantly curtailed the magnitude of the subsequent eosinophil infiltrate Enumeration of eosinophils from the ear tissue of sensitized mice revealed a similar trend with a nearly fivefold increase in eosinophils as compared with unsensitized mice (not depicted).…”

Section: And E)mentioning

confidence: 99%

IgE-activated basophils regulate eosinophil tissue entry by modulating endothelial function

Cheng¹,

Sullivan²,

Retana³

et al. 2015

J Cell Biol

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Vertebrate immunity has evolved a modular architecture in response to perturbations. Allergic inflammation represents such a module, with signature features of antigen-specific IgE and tissue eosinophilia, although the cellular and molecular circuitry coupling these responses remains unclear. Here, we use genetic and imaging approaches in models of IgEdependent eosinophilic dermatitis to demonstrate a requisite role for basophils. After antigenic inflammation, basophils initiate transmigration like other granulocytes but, upon activation via their high-affinity IgE receptor, alter their migratory kinetics to persist at the endothelium. Prolonged basophil-endothelial interactions, in part dependent on activation of focal adhesion kinases, promote delivery of basophil-derived IL-4 to the endothelium and subsequent induction of endothelial vascular cell adhesion molecule-1 (VCAM-1), which is required for eosinophil accumulation. Thus, basophils are gatekeepers that link adaptive immunity with innate effector programs by altering access to tissue sites by activation-induced interactions with the endothelium.

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“…Tape stripping experiments have clearly been shown to shift the TH1/TH2 balance of the adaptive immune response-though the direction of that shift is not absolute. Several studies associate scratching and tape-stripping with exacerbation of TH2 biased allergic immunity 30,34,35 , while other studies evidence a TH1 skewing effect of tape striping 28,36 . So while it's clear that the TH1/TH2 balance is altered via skin disruption, and that this balance is critical for disease outcomes, both relationships appear to be complex, model, and timepoint dependent.…”

Section: The Immunomodulatory Outcomes Of Skin Barrier Disruptionmentioning

confidence: 99%

The itch-scratch reflex generates protective immunity

Radjavi

Lebeau

2019

Preprint

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Itch: its complex neurobiology, its exquisite evolutionary conservation, and even the undeniably euphoric sensation of the scratch it evokes, are all suggestive of a productive physiological function. Nevertheless, we still struggle to answer (or altogether overlook) the basic question of why we itch in the first place. Here, we propose a simple hypothesis: the purpose of itch sensation is to evoke scratching behavior, which in turn boosts protective immunity against the broad range of pathogenic challenges that enter at the skin. We propose that the key function of itch induced scratching is to physically disrupt the skin, serving as a "mechanical adjuvant" that amplifies and directs immune responses to the precise site of potential pathogen entry. As proof of principle, we show that the potent adjuvanticity of itch inducing Compound 48/80 is dependent on this agent's ability to elicit scratching behavior.

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Mechanical Injury Polarizes Skin Dendritic Cells to Elicit a Th2 Response by Inducing Cutaneous TSLP Expression

Cited by 6 publications

References 16 publications

A low inflammatory, Langerhans cell-targeted microprojection patch to deliver ovalbumin to the epidermis of mouse skin

A low inflammatory, Langerhans cell-targeted microprojection patch to deliver ovalbumin to the epidermis of mouse skin

IgE-activated basophils regulate eosinophil tissue entry by modulating endothelial function

The itch-scratch reflex generates protective immunity

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