Abstract

Asthma is a heterogeneous disease that affects approximately 300 million people worldwide, largely in developed countries. The etiology of the disease is poorly understood, but is likely to involve specific innate and adaptive responses to inhaled microbial components that are found in allergens. Fungal-derived allergens represent a major contributing factor in the initiation, persistence, exacerbation, and severity of allergic asthma. C-type lectin like receptors, such as dectin-1, dectin-2, DC-specific intercellular adhesion molecule 3-grabbing nonintegrin, and mannose receptor, recognize many fungal-derived allergens and other structurally similar allergens derived from house dust mites (HDM). In some cases, the fungal derived allergens have been structurally and functionally identified alongside their respective receptors in both humans and mice. In this review, we discuss recent understanding on how selected fungal and HDM derived allergens as well as their known or unknown receptors shape allergic airway diseases.

Highlights

  • Over the past few decades, it has become widely accepted that fungi can contribute negatively to many aspects of human health and the particular focus on this review is allergic airway diseases

  • These characteristics are similar to allergic asthmatics sensitized to various allergens such as those derived from house dust mites (HDM), pollen, cockroach, etc

  • Downstream, Bcl3, an NFkB subunit interferes with p50–p65 subunit dimerization and binds to p65 binding site and translocate to the nucleus, thereby repressing NFkB-dependent transcription of pro-inflammatory genes [62]. Whether this fucose/DC-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN) signaling and Th2 differentiation is a common mechanism for all fucose decorated allergens such as those derived from fungi or HDM, and how DC-SIGN selectively engages different carbohydrate, is currently unclear and requires further investigation

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Summary

Frontiers in Immunology

Asthma is a heterogeneous disease that affects approximately 300 million people worldwide, largely in developed countries. The etiology of the disease is poorly understood, but is likely to involve specific innate and adaptive responses to inhaled microbial components that are found in allergens. Fungal-derived allergens represent a major contributing factor in the initiation, persistence, exacerbation, and severity of allergic asthma. C-type lectin like receptors, such as dectin-1, dectin-2, DC-specific intercellular adhesion molecule 3-grabbing nonintegrin, and mannose receptor, recognize many fungal-derived allergens and other structurally similar allergens derived from house dust mites (HDM). The fungal derived allergens have been structurally and functionally identified alongside their respective receptors in both humans and mice. We discuss recent understanding on how selected fungal and HDM derived allergens as well as their known or unknown receptors shape allergic airway diseases

INTRODUCTION
Surfactant protein A and D
Chitin Detecting CLRs
Mannose Receptor
Surfactant Proteins A and D
Findings
CONCLUDING REMARKS
Full Text
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