Abstract
Programmed cell death 1 (PD-1) and its ligands PD-L1 and PD-L2 are receptors that act in co-stimulatory and coinhibitory immune responses. Signaling the PD-1/PD-L1 or PD-L2 pathway is essential to regulate the inflammatory responses to infections, autoimmunity, and allergies, and it has been extensively studied in cancer. Allergic diseases include asthma, rhinoconjunctivitis, atopic dermatitis, drug allergy, and anaphylaxis. These overactive immune responses involve IgE-dependent activation and increased CD4+ T helper type 2 (Th2) lymphocytes. Recent studies have shown that PD-L1 and PD-L2 act to regulate T-cell activation and function. However, the main role of PD-1 and its ligands is to balance the immune response; however, the inflammatory process of allergic diseases is poorly understood. These immune checkpoint molecules can function as a brake or a kick-start to regulate the adaptive immune response. These findings suggest that PD-1 and its ligands may be a key factor in studying the exaggerated response in hypersensitivity reactions in allergies. This review summarizes the current understanding of the role of PD-1 and PD-L1 and PD-L2 pathway regulation in allergic diseases and how this immunomodulatory pathway is currently being targeted to develop novel therapeutic immunotherapy.
Highlights
Allergic diseases are characterized by hyperreactive immune responses to otherwise innocuous antigens in the general population, the incidence and prevalence of which are increasing worldwide, in the developed world
Soluble Programmed cell death 1 (PD-1), programmed death (PD)-L1 and PD-L2 after segmental allergen challenge (SAC) were not expressed; PD-L1 expression in Peripheral blood lymphocytes and DCs (pDCs) after high-affinity IgE receptor cross-linking in bronchoalveolar lavage fluid (BALF) was significantly associated with PD-L1 expression in pDCs when IgE was inoculated
Using the endobronchial allergen challenge (EAC) in asthmatic patients, Bratke et al demonstrated a small decrease in endobronchial PD-1+ CD4+ T cells was accompanied by an increase in PD-L1 expression on endobronchial myeloid DCs (mDCs) and pDCs, 24 h after AEC, which may favor Th2 inflammation [81]
Summary
Allergic diseases are characterized by hyperreactive immune responses to otherwise innocuous antigens in the general population, the incidence and prevalence of which are increasing worldwide, in the developed world. Antigen-presenting cells (APCs) become activated, and epithelial alarmins (IL-25, IL-31, IL-33, and TSLP) are released due to activation of the airway epithelial cells in response to allergens [7], leading to activation of Th2/mast cell/eosinophil/eosinophil-mediated allergic pathology, including IL-4 and IL-5. Another pathway is the Th1/Th17/neutrophilmediated response to chronic innate immune activation and irreversible airway obstruction [8,9]. In chronic asthma, Th1 and Th2 cytokines contribute to airway wall remodeling Another group of cells that respond to environmental signals are group 2 innate lymphoid cells that exhibit a dynamic phenotype in allergic airway inflammation [10]. This review provides an overview of the role of PD-1 and its ligands in allergic disease
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