About this Research Topic
Similar to Th1 responses, differentiation of naive T cells into Th2 cells in response to allergens also involves activation of the innate immune system. Activation of innate cells is mainly mediated by pattern-recognition receptors (PRRs) (e.g. Toll-like receptors, TLRs; C-type lectin receptors, CLRs; NOD-like receptors, NLRs), which form the sensory interface of the innate immune system.
Both the allergens themselves and danger signals present in the allergen source or in the environment have been shown to directly activate PRRs. PRR activation on dendritic cells (DCs) may directly promote the induction of inflammatory TH2 cells. However, PRRs are also expressed on epithelial cells and their activation leads to secretion of thymic stromal lymphopoietin (TSLP), GM-CSF, and distinct cytokines, which can indirectly trigger DC activation. Moreover, viral infections, tissue damage, and the release of reactive oxygen species have great influence on the expression levels of PRRs, and influence thresholds and epithelial responsiveness towards external stimuli.
The aim of this topic is to provide an overview of ongoing investigations and to integrate current knowledge on interactions between allergen and allergenic sources with components of the innate immune system leading to Th2-polarized and IgE-mediated adaptive responses.
Submissions of Original Research, Methods, Perspective, Mini-Review, and Review articles are welcome. The subtopics of interest include, but are not limited to:
• Epithelial innate immune responses to allergens and allergenic sources
• Innate immune activation of dendritic cells by allergen and allergenic sources
• The role of innate immune cells in the initiation and maintenance of allergen-specific T cell responses
• Animal models for studying innate immune responses to allergens and allergenic sources
• The interplay between environmental adjuvants and innate immunity in allergic sensitization
• The role of innate immune responses to respiratory virus and bacteria in allergic sensitization
• Molecular structures involved in innate immune responses to allergens and allergenic sources
Both the allergens themselves and danger signals present in the allergen source or in the environment have been shown to directly activate PRRs. PRR activation on dendritic cells (DCs) may directly promote the induction of inflammatory TH2 cells. However, PRRs are also expressed on epithelial cells and their activation leads to secretion of thymic stromal lymphopoietin (TSLP), GM-CSF, and distinct cytokines, which can indirectly trigger DC activation. Moreover, viral infections, tissue damage, and the release of reactive oxygen species have great influence on the expression levels of PRRs, and influence thresholds and epithelial responsiveness towards external stimuli.
The aim of this topic is to provide an overview of ongoing investigations and to integrate current knowledge on interactions between allergen and allergenic sources with components of the innate immune system leading to Th2-polarized and IgE-mediated adaptive responses.
Submissions of Original Research, Methods, Perspective, Mini-Review, and Review articles are welcome. The subtopics of interest include, but are not limited to:
• Epithelial innate immune responses to allergens and allergenic sources
• Innate immune activation of dendritic cells by allergen and allergenic sources
• The role of innate immune cells in the initiation and maintenance of allergen-specific T cell responses
• Animal models for studying innate immune responses to allergens and allergenic sources
• The interplay between environmental adjuvants and innate immunity in allergic sensitization
• The role of innate immune responses to respiratory virus and bacteria in allergic sensitization
• Molecular structures involved in innate immune responses to allergens and allergenic sources
Keywords: allergens, allergies, immunology, innate immunity, host responses, allergic sensitization, immune responses, molecular allergology
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
