Abstract
Asthma is a chronic inflammatory disease affecting the airway, and it is characterized by a wheezing breathing sound, variable airflow obstruction and the presence of inflammatory cells in the submucosa of the bronchi. Viral infection, pollutants and sensitivity to aeroallergens damage the epithelium from childhood, which causes asthma. The pathogenesis of asthma includes pathways of innate stimulation by environmental microbes and irritant pathogens. Damaged epithelial cells produce thymic stromal lymphopoietin (TSLP) and stimulate myeloid dendritic cell maturation through the thymic stromal lymphopoietin receptor (TSLPR) heterocomplex. TSLP-activated myeloid dendritic cells promote naive CD4+ T cells to differentiate into T helper type 2 (Th2) phenotype CD4+ T cells. Re-exposure to allergens or environmental stimuli causes an adaptive immune response. TSLP-activated dendritic cells expressing the OX40 ligand (OX40L; CD252) trigger naive CD4+ T cells to differentiate into inflammatory Th2 effector cells secreting the cytokines interleukin-4, 5, 9, and 13 (IL-4, IL-5, IL-9 and IL-13), and the dendritic cells (DCs) promote the proliferation of allergen-specific Th2 memory cells. Allergen presentation by Th2 cells through its interaction with their receptors in the presence of major histocompatibility complex (MHC) class II on B cells and through costimulation involving CD40 and CD40L interactions results in immunoglobulin class switching from IgM to IgE. DCs and other blood cell subsets express the TSLPR heterocomplex. The regulatory mechanism of the TSLPR heterocomplex on these different cell subsets remains unclear. The TSLPR heterocomplex is composed of the IL-7Rα chain and TSLPR chain. Moreover, two isoforms of TSLP, short isoform TSLP (sfTSLP) and long isoform TSLP (lfTSLP), have roles in atopic and allergic development. Identifying and clarifying the regulation of TSLPR and IL-7Rα in pediatric asthma are still difficult, because the type of blood cell and the expression for each blood cell in different stages of atopic diseases are poorly understood. We believe that further integrated assessments of the regulation mechanism of the TSLP–TSLPR heterocomplex axis in vitro and in vivo can provide a faster and earlier diagnosis of pediatric asthma and promote the development of more effective preventive strategies at the onset of allergies.
Highlights
Asthma is a chronic inflammatory respiratory disease leading to variable airflow obstruction
In allergen-specific Th2 memory cells, the major histocompatibility complex (MHC) class II-associated allergen interacts with the receptors on B cells and costimulates CD40 and CD40L interactions, resulting in immunoglobulin class switching from IgM to immunoglobulin E (IgE) [6]
This results in the selective expansion of T lymphocytes, which secrete cytokines encoded on chromosome 5q31–33, including interleukins IL-3, IL-4, IL-5, IL-9 and IL-13, and the granulocyte macrophage colony-stimulating factor (GM-CSF) that causes airway smooth muscle contraction and vasodilatation and increased vascular permeability and mucous secretion [1,6]
Summary
Asthma is a chronic inflammatory respiratory disease leading to variable airflow obstruction. In allergen-specific Th2 memory cells, the MHC class II-associated allergen interacts with the receptors on B cells and costimulates CD40 and CD40L interactions, resulting in immunoglobulin class switching from IgM to IgE [6] This results in the selective expansion of T lymphocytes ( the Th2 type), which secrete cytokines encoded on chromosome 5q31–33, including interleukins IL-3, IL-4, IL-5, IL-9 and IL-13, and the granulocyte macrophage colony-stimulating factor (GM-CSF) that causes airway smooth muscle contraction and vasodilatation and increased vascular permeability and mucous secretion [1,6]. The TSLP–TSLPR heterocomplex axis may play a fundamental role in the innate–adaptive interface in the pathology of asthma (Figure 1)
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