No Abstract available.
Hypersensitivity* ; Immunity, Innate*

Group 3 innate lymphoid cells (ILC3) are an ILC subset that is characterized by the expression of retinoic acid-related orphan nuclear receptor γt (RORγt) and interleukin 22 (IL-22). This review summarizes the role of ILC3 in coordinating innate immunity and adaptive immunity based on current research and elaborate the significance of ILC3 from the perspective of immune system evolution. In addition, based on immune-related functions, we propose a possible time when ILC3 appears in the evolution of the immune system. And then, the research limitations and prospects are discussed.
Immunity, Innate ; Lymphocytes ; Tretinoin

Cell-mediated immune response is an important part of machinery in maintaining the body's homeostasis. After the innate immune system selectively activates the adaptive immune system, the cell-mediated immunity exerts its killing and clearance functions. Therefore, evaluating the level of cell-mediated immune response is crucial in the diagnosis and treatment of cancer, monitoring the immune status after organ transplantation, diagnosing and preventing viral diseases, and evaluating the effectiveness of vaccines and other areas. From the initial overall assessment of the immune effects in vivo to the precise detection of the number and function of multiple immune cells, the evaluation methods of cell-mediated immune response have greatly advanced. However, cell-mediated immune response involves multiple levels in the body, and it's difficult to choose the numerous detection methods available. The article systematically compares the evaluation methods of cell-mediated immune response at four different levels: the organism, the tissue and organ, the immune cells and the immune molecules, with the aim to facilitate the applications of related technologies.
Humans ; Immunity, Cellular ; Neoplasms/therapy* ; Immunity, Innate

Most of perinatological phenomenona and diseases are closely related with immune reaction. Most of initial immune responses occur through innate immunity and most causes, such as mechanical damage, hypoxia, and hyperoxia, are self and microorganisms are non-self, all of which are related with immune reaction concept. However, researches on perinatology are mainly focused on specific one or two causes of perinatal diseases, so often there is limitation to understand the basic concepts and phenomenona of the perinatal diseases. Through understanding of immune reaction concept, we can apply immune reaction theory to researches in perinatology and we can understand phenomenona in perinatology through knowledge of immune reaction. Therefore it is essential to understand historical development of immunology and concept of immune reaction for researches and treatment of perinatology.
Allergy and Immunology ; Anoxia ; Hyperoxia ; Immunity, Innate ; Perinatology*

Autophagy is a self-degradative process that removes misfolded or aggregated proteins, clears damaged organelles, as well as eliminates intracellular pathogens playing a role in innate immunity. Mycobacterium abscessus (M. abscessus) has been reported as a causative organism in nearly 80% of the rapid growing mycobacteria (RGM) pulmonary disease. The strain exhibits two different colony types: the smooth (S) one which is considered wild-type and the rough (R) one which is the mutated strain. In accordance to the colony morphology, the S and R types display varying autophagic responses in the host cells with the R type inducing elevated autophagy compared to the S type. The major difference in the autophagy could be based on the bioactive molecules exposed on the surface of the S and R types. Though autophagy has a vital role to play in the clearance of intracellular pathogens, very little is known on the autophagy induced by M. abscessus. It has been known that the intracellular pathogens employ different strategies to evade the autophagic pathway and to survive within the host cells. This review summarizes the most up-to-date findings on autophagy induced by M. abscessus morphotypes and how M. abscessus evades the autophagic machinery to divide and thrive inside the host cells. In addition, the prospects of autophagic machinery in devising new anti-infective strategies against mycobacterial infection is also been discussed.
Autophagy* ; Immunity, Innate ; Lung Diseases ; Mycobacterium* ; Organelles

Autophagy is a self-degradative process that removes misfolded or aggregated proteins, clears damaged organelles, as well as eliminates intracellular pathogens playing a role in innate immunity. Mycobacterium abscessus (M. abscessus) has been reported as a causative organism in nearly 80% of the rapid growing mycobacteria (RGM) pulmonary disease. The strain exhibits two different colony types: the smooth (S) one which is considered wild-type and the rough (R) one which is the mutated strain. In accordance to the colony morphology, the S and R types display varying autophagic responses in the host cells with the R type inducing elevated autophagy compared to the S type. The major difference in the autophagy could be based on the bioactive molecules exposed on the surface of the S and R types. Though autophagy has a vital role to play in the clearance of intracellular pathogens, very little is known on the autophagy induced by M. abscessus. It has been known that the intracellular pathogens employ different strategies to evade the autophagic pathway and to survive within the host cells. This review summarizes the most up-to-date findings on autophagy induced by M. abscessus morphotypes and how M. abscessus evades the autophagic machinery to divide and thrive inside the host cells. In addition, the prospects of autophagic machinery in devising new anti-infective strategies against mycobacterial infection is also been discussed.
Autophagy* ; Immunity, Innate ; Lung Diseases ; Mycobacterium* ; Organelles

Hepatitis C ; immunology ; pathology ; Immunity, Innate

Humans ; Immunity, Innate ; Lymphocytes ; Cardiovascular Diseases ; Cytokines

Group 3 innate lymphoid cells (ILC3) as a family member of innate lymphoid cells (ILCs), have been defined as novel innate immune cells in the past decade. ILC3 include a variety of heterogenous subsets with different phenotypes and functions, which are mainly distributed in barrier organs such as the intestine, lung and skin. They play an important role in immune regulation, tissue repair and lymphoid tissue formation. However, in various inflammatory diseases, ILC3 become dysregulated and participate in the pathogenesis through secreting a series of cytokines such as interleukin (IL)-17, IL-22, interferon-γ (IFN-γ) and granulocyte-macrophage colony-stimulating factor (GM-CSF) to modulate other immune cells and induce the formation of ectopic lymphoid structures. Therefore, it is of great significance to explore the phenotype and function of ILC3 in order to advance the understanding of inflammatory diseases and find new therapeutic targets. In this article, the phenotypic characteristics, biological functions and research progress of ILC3 in inflammatory diseases were reviewed.
Cytokines ; Immunity, Innate ; Interferon-gamma ; Intestines ; Lymphocytes

Chronic rhinosinusitis (CRS) is characterized by persistent symptomatic inflammation of the nasal and paranasal sinus mucosa resulting from the interaction of multiple host and environmental factors. Although the etiology of CRS remains a matter of vigorous debate, research into CRS has implicated that the epithelium plays an important role as both a mediator and a regulator of innate and adaptive immune responses, as well as the transition from innate immunity to adaptive immunity. Recently, alterations of epithelial barrier functions, dysregulation of the innate immune system and inappropriate activation of the adaptive immune system have been identified as active processes in the pathogenesis of CRS. This review summarizes recent emerging evidence regarding the underlying pathogenic mechanism in CRS, which highlights the increasing recognition of the epithelium as a central factor in CRS etiology and pathogenesis.
Adaptive Immunity ; Epithelium* ; Immune System ; Immunity, Innate ; Inflammation ; Mucous Membrane