Crosstalk between ILC2s and Th2 CD4+ T Cells in Lung Disease.

Cytokine secretion, such as interleukin-4 (IL-4), IL-5, IL-9, IL-13, and amphiregulin (Areg), by type 2 innate lymphoid cells (ILC2s) is indispensable for homeostasis, remodeling/repairing tissue structure, inflammation, and tumor immunity. Often viewed as the innate cell surrogate of T helper type 2 (Th2) cells, ILC2s not only secrete the same type 2 cytokines, but are also inextricably related to CD4+T cells in terms of cell origin and regulatory factors, bridging between innate and adaptive immunity. ILC2s interact with CD4+T cells to play a leading role in a variety of diseases through secretory factors. Here, we review the latest progress on ILC2s and CD4+T cells in the lung, the close relationship between the two, and their relevance in the lung disease and immunity. This literature review aids future research in pulmonary type 2 immune diseases and guides innovative treatment approaches for these diseases.

A crosstalk between type 2 innate lymphoid cells and alternative macrophages in lung development and lung diseases (Review).

Type 2 innate lymphoid cells (ILC2s) are important innate immune cells that are involved in type 2 inflammation, in both mice and humans. ILC2s are stimulated by factors, including interleukin (IL)­33 and IL­25, and activated ILC2s secrete several cytokines that mediate type 2 immunity by inducing profound changes in physiology, including activation of alternative (M2) macrophages. M2 macrophages possess immune modulatory, phagocytic, tissue repair and remodeling properties, and can regulate ILC2s under infection. The present review summarizes the role of ILC2s as innate cells and M2 macrophages as anti­inflammatory cells, and discusses current literature on their important biological significance. The present review also highlights how the crosstalk between ILC2s and M2 macrophages contributes to lung development, induces pulmonary parasitic expulsion, exacerbates pulmonary viral and fungal infections and allergic airway diseases, and promotes the development of lung diseases, such as pulmonary fibrosis, chronic obstructive pulmonary disease and carcinoma of the lungs.

Group 2 innate lymphoid cells (ILC2s): The spotlight in asthma pathogenesis and lung tissue injury

Asthma is a heterogeneous disease with ranging etiology and severity. Asthma is a disease of chronic inflammation of the airways, with clinical symptoms of wheezing, breathlessness, cough, and chest tightness manifested as chronic fixed or variable airflow obstruction and airway hyperresponsiveness that predispose the airway epithelium to repeated injury, repair, and regeneration. In recent years, innate lymphoid cells (ILC1, ILC2, and ILC3) have been discovered. The predominant ILC type found in the lung tissue is group 2 innate lymphoid cells (ILC2s). Upon damage to the airway epithelium mediating the release of epithelial cytokines (TSLP, IL-33, and IL-25) ensued the activation of ILC2 in an antigen-independent manner. Activated ILC2 produces a significant amount of type 2 cytokines (IL-4, IL-5, IL-9, and IL-13), altogether contributing to type 2 inflammation in the airways. ILC2s are mediators of type 2 immunity for many type 2 inflammatory diseases such as asthma, since ILC2s were reported to play an important role in asthma pathogenesis. Here we discuss the role of ILC2 in the development of asthma and ILC2 effector cytokines (IL-4, IL-5, and IL-13) contributing to airway epithelial structural changes (AU)

Group 2 innate lymphoid cells (ILC2s): The spotlight in asthma pathogenesis and lung tissue injury.

Asthma is a heterogeneous disease with ranging etiology and severity. Asthma is a disease of chronic inflammation of the airways, with clinical symptoms of wheezing, breathlessness, cough, and chest tightness manifested as chronic fixed or variable airflow obstruction and airway hyperresponsiveness that predispose the airway epithelium to repeated injury, repair, and regeneration. In recent years, innate lymphoid cells (ILC1, ILC2, and ILC3) have been discovered. The predominant ILC type found in the lung tissue is group 2 innate lymphoid cells (ILC2s). Upon damage to the airway epithelium mediating the release of epithelial cytokines (TSLP, IL-33, and IL-25) ensued the activation of ILC2 in an antigen-independent manner. Activated ILC2 produces a significant amount of type 2 cytokines (IL-4, IL-5, IL-9, and IL-13), altogether contributing to type 2 inflammation in the airways. ILC2s are mediators of type 2 immunity for many type 2 inflammatory diseases such as asthma, since ILC2s were reported to play an important role in asthma pathogenesis. Here we discuss the role of ILC2 in the development of asthma and ILC2 effector cytokines (IL-4, IL-5, and IL-13) contributing to airway epithelial structural changes.