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Allergic rhinitis (AR) is a type I allergic reaction, which mediated by immunoglobulin E immediately when an individual with a special constitution is exposed to a same allergen for second time, whose pathogenesis has not been clarified yet, and closely related to genes, immune cells and cytokines. Pathogenesis of AR become more deeper and more accurate due to rapid develop-ment of molecular biology and second-generation gene sequencing technology. Current studies have found that miR-155 and transcription factor GATA3 have important regulatory effects on occurrence and development of AR, then affect dominant differentiation of CD4+T lymphocytes and proliferation of ILC2. This article discusses and reviews pathogenesis of AR, which mainly focuses on miR-155/GATA3 pathway and effects of related upstream genes and downstream regulatory substances. [ABSTRACT FROM AUTHOR]

The type Ⅱ inflammatory response is primarily mediated by type 2 immune cells and cytokines, such as helper 2 cells （Th2） and group 2 innate lymphoid cells (ILC2), along with IL-4, IL-5 and IL-13. This response plays crucial roles in humoral immunity, parasite defense, toxin neutralization, tissue damage repair and regeneration. However, type-Ⅱ immune response can also contribute to the development of diseases. Currently, type Ⅱ inflammation is recognized to have physiological and pathological implications in the skin, respiratory tract, digestive tract and adipose tissues. Moreover, it serves as a major cause of allergic diseases. Due to its unique immune microenvironment, the respiratory tract exhibits a high prevalence of type Ⅱ inflammation encompassing chronic sinusitis, allergic rhinitis, allergic asthma, allergic bronchopulmonary aspergillosis, and chronic obstructive pulmonary disease with eosinophilia among others. This review will focus on the research progress concerning Th2 and ILC2 cells in allergic pulmonary inflammation as well as targeted therapy for allergic diseases. [ABSTRACT FROM AUTHOR]

Objective: To observe the effect of glucocorticoids on type 2 innate lymphoid cells (ILC2s) in eosinophilic asthma (EA), and to explore the effect of glucocorticoids on ILC2s. Methods: From June 2021 to June 2022, the research subjects were recruited in the Fifth Affiliated Hospital of Sun Yat-sen University. The general data, induced sputum, blood indexes and pulmonary function of the research subjects were collected. The ratio of ILC2s（CD45+Lin-CD127+CD294+） in peripheral blood PBMC were detected by flow cytometry. Cytokines IL-5 and IL-13 in serum were tested by ELISA. The EA patients were treated with glucocorticoid for 3 months.C57BL/6J mice were sensitized by intraperitoneal injection of chicken ovalbumin (Ovalbumin, OVA) with 20 μg, and then was stimulated by inhalation of 1% OVA, which was the EA asthma model. The negative control (NC) group mice were treated with the same volume of PBS. The number of eosinophils was counted; The lung tissue of the mice in each group was stained with HE to observe the inflammation. Flow cytometry was used to detect the changes in the proportion of ILC2s in peripheral blood PBMC and bronchoalveolar lavage in each group. After glucocorticoid treatment, in the EA mouse model, the inflammation of lung and ILC2s in peripheral blood and bronchoalveolar lavage fluid were observed; ILC2s were isolated from lung tissue, and the expression of related proteins was evaluated by western blot. Results: The proportion of ILC2s, EOS, IL-5 and IL-13 were increased in the EA group. After glucocorticoids therapy for 3months, the proportion of ILC2s, IL-5 and IL-13 were significantly decreased. In addition, in EA mouse model, ILC2s in PBMC and BALF, EOS in BALF and type 2 cytokines IL-5 and IL-13 in serum were increased, but the lung Inflammation was worsened compared with NC. After glucocorticoid treatment, inflammation of lung was alleviated and EOS, ILC2s, IL-5 and IL-13 were decreased. Furtherly, in vitro stimulation of isolated ILC2s found that JAK/STAT protein were proved to be involved in regulating ILC2s activity under the glucocorticoid treatment. Conclusion: Glucocorticoid administration could be effective in treating EA by regulating ILC2s via JAK-STAT signaling pathways, which provides a new direction for the mechanism of hormone therapy for eosinophilic asthma. [ABSTRACT FROM AUTHOR]

The incidence of allergic asthma has been increasing year by year. It is estimated that there are more than 300 million illnesses. It is associated with increased IgE, mast cell activation, airway hyperreactivity, excessive mucus production, and airway remodeling. The traditional view is that allergic asthma is associated with allergic reactions involving T helper type 2 (Th2) cells. Recent studies have found that different subsets of CD4+ T cells (Th17, Th9) as well as innately immunized cells such as mast cells and innate lymphocyte type 2 (ILC2s) are able to produce cytokine IL-9, leading to asthma. Th9 cells develop from nave T cells to IL-9 producing cells in the presence of IL-4 and TGF-β. IRF4, GATA3, a basic leucine zipper transcription factor, several transcription factors downstream of BATF and IL-4 such as signal transduction and STAT6-activated NFAT are activated. In addition, the transcription factor PU.1 downstream of TGF-β signaling appears to be also critical for the development of Th9 cells. IL-9 is a pleiotropic cytokine that affects the function of different target cells such as T cells, B cells, mast cells and airway epithelial cells by activating STAT1, STAT3 and STAT5. Due to its versatility, IL-9 has been shown to be involved in several diseases such as cancer, autoimmunity and other pathogenmediated immunomodulatory diseases. This article reviews the role of Th9 and IL-9producing cells in allergic asthma., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)