Expression of CD226 in the small intestinal group 3 innate lymphoid cells (ILC3) in mice / 细胞与分子免疫学杂志

Objective To observe the expression of adhesion molecule CD226 on the small intestinal group 3 innate lymphoid cells (ILC3) in mice. Methods The bioinformatics was used to analyze the expression of CD226 on murine ILCs. Small intestinal mucosal lamina propria lymphocytes (LPL) were isolated from wild-type C57BL/6J mice, and the expression of CD226 on ILC1 and ILC3 was detected by flow cytometry. A mouse model of dextran sulfate sodium (DSS)-induced colitis was constructed to observe the changes in the expression of CD226 on ILC3. Results Both ILC1 and ILC3 in the mice small intestine expressed CD226 molecules; the proportion of ILC3 was reduced, while the expression level of CD226 on ILC3 was increased in the colitis model. Conclusion CD226 is expressed on the small intestines of mice, and although the proportion of ILC3 decreases in the DSS-induced colitis, the expression of CD226 on ILC3 increases.

Progress in research of epidemiology of 2019-nCoV reinfection / 中华流行病学杂志

Continuous evolution of Omicron variant of 2019-nCoV has resulted in a rapid and simultaneous emergences of novel sub-variants with increased immune escape ability, higher reinfection risk and shorter time interval between infections. Compared with the first infection, the reinfection would still pose exceed risk to people's health although the clinical manifestations of the reinfection might be milder and the risk for severe illness or death is lower. The reinfection is highly associated with people's vaccination status, immunity level, age, working and residential factors. Those who have not received 2019-nCoV vaccination, the elderly and those with comorbidities, especially the previous 2019-nCoV patients with severe/critical illness, are at high risk for the reinfection. Booster doses of vaccine might play an additional role in the prevention of the reinfection and severe illness on the basis of natural immunity.

Immunogenic molecules associated with gut bacterial cell walls: chemical structures, immune-modulating functions, and mechanisms

Interactions between gut microbiome and host immune system are fundamental to maintaining the intestinal mucosal barrier and homeostasis. At the host-gut microbiome interface, cell wall-derived molecules from gut commensal bacteria have been reported to play a pivotal role in training and remodeling host immune responses. In this article, we review gut bacterial cell wall-derived molecules with characterized chemical structures, including peptidoglycan and lipid-related molecules that impact host health and disease processes via regulating innate and adaptive immunity. Also, we aim to discuss the structures, immune responses, and underlying mechanisms of these immunogenic molecules. Based on current advances, we propose cell wall-derived components as important sources of medicinal agents for the treatment of infection and immune diseases.

The I226R protein of African swine fever virus inhibits the cGAS-STING-mediated innate immune response / 生物工程学报

This study aimed to explore the mechanism of how African swine fever virus (ASFV) I226R protein inhibits the cGAS-STING signaling pathway. We observed that I226R protein (pI226R) significantly inhibited the cGAS-STING-mediated type Ⅰ interferons and the interferon-stimulated genes production by dual-luciferase reporter assay system and real-time quantitative PCR. The results of co-immunoprecipitation assay and confocal microscopy showed that pI226R interacted with cGAS. Furthermore, pI226R promoted cGAS degradation through autophagy-lysosome pathway. Moreover, we found that pI226R decreased the binding of cGAS to E3 ligase tripartite motif protein 56 (TRIM56), resulting in the weakened monoubiquitination of cGAS, thus inhibiting the activation of cGAS and cGAS-STING signaling. In conclusion, ASFV pI226R suppresses the antiviral innate immune response by antagonizing cGAS, which contributes to an in-depth understanding of the immune escape mechanism of ASFV and provides a theoretical basis for the development of vaccines.

Advances in innate immune responses induced by Mycoplasma hyopneumoniae infection / 生物工程学报

Mycoplasma hyopneumoniae is the pathogen causing swine mycoplasmal pneumonia. The lack of well-established animal models of M. hyopneumoniae infection has delayed the progress of M. hyopneumoniae-related anti-infection immunity studies. This paper reviews the inflammatory response, the recognition of M. hyopneumoniae by the innate immune system, and the role of innate immune cells, complement system, antimicrobial peptides, autophagy, and apoptosis in M. hyopneumoniae infection. The aim was to elucidate the important roles played by the components of the innate immune system in the control of M. hyopneumoniae infection, and prospect key research directions of innate immune response of M. hyopneumoniae infection in the future.

Advances in methodologies for evaluating cell-mediated immune responses / 生物工程学报

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.

Intestinal and lung inflammatory group 2 innate lymphoid cells (iILC2s) and their related cytokines in chronic obstructive pulmonary disease / 细胞与分子免疫学杂志

Objective To investigate the relationship between intestinal inflammatory group 2 innate lymphoid cells (iILC2s) and lung ILC2s and its inflammatory response in chronic obstructive pulmonary disease (COPD). Methods Mouse COPD model was established by smoking method. The mice were randomly divided into normal group and COPD group. HE staining was used to detect the pathological changes in lung and intestine tissues of mice in normal group and COPD group, and the contents of natural ILC2s(nILC2s) and iILC2s cells were measured by flow cytometry. Wright-Giemsa staining was used to measure the number of immune cells in the bronchoalveolar lavage fluid (BALF) of mice in normal group and COPD group, and the concentration of IL-13 and IL-4 was detected by ELISA. Results In COPD mice, epithelial cells of the lung and intestinal tissues exhibited pathological hyperplasia, partial atrophy or deletion, inflammatory cell infiltration, increased pathological score and significantly increased neutrophils, monocytes, and lymphocytes in BALF. Lung iILC2s, intestinal nILC2s and iILC2s were increased significantly in the COPD group. The contents of IL-13 and IL-4 in BALF were significantly increased. Conclusion The increase of iILC2s and their related cytokines in COPD lung may be related to intestinal inflammatory ILC2s.

The role of group 3 innate lymphoid cells(ILC3) in the evolution of the immune system: An update / 细胞与分子免疫学杂志

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.

The role of group 2 innate lymphoid cells (ILC2) in respiratory allergic diseases: An update / 细胞与分子免疫学杂志

Group 2 innate lymphoid cells (ILC2s) are the "mirror cells" of Th2 cells. Although the total cell number of ILC2s is far less than that of CD4+ Th2 cells in the body, the activated ILC2s have a more powerful biological activity than CD4+ Th2 cells and can rapidly enhanced Th2-cell inflammatory reaction. It plays an important role in the pathogenesis of allergic respiratory diseases. The transmitters that activate ILC2s include inflammatory cytokines (IL-33, IL-25, TSLP, IL-4, IL-9), lipid transmitters (prostaglandins, leukotrienes), and other activating transmitters (ICOS, Complement C3a, neuropeptide receptor, vasoactive intestinal peptide and calcitonin gene-related peptide, etc). Activated ILC2s produce large amounts of IL-4, IL-5, IL-9, IL-13, and amphiregulin and other inflammatory mediators, and induce airway hyperresponsiveness, mucus secretion and airway remodeling and other respiratory allergic reactions. Therefore, respiratory allergic diseases, especially steroid-dependent asthma, could be treated potentially by inhibiting the activation of ILC2s. Hereby, we summarized the immunobiology of ILC2s, the initiation of ILC2s in allergic inflammation, the relationship between ILC2s and respiratory allergic diseases, and the recent advances in biological agents targeted by ILC2s.

Modulation of type I interferon signaling by natural products in the treatment of immune-related diseases / 中国天然药物

Type I interferon (IFN) is considered as a bridge between innate and adaptive immunity. Proper activation or inhibition of type I IFN signaling is essential for host defense against pathogen invasion, tumor cell proliferation, and overactive immune responses. Due to intricate and diverse chemical structures, natural products and their derivatives have become an invaluable source inspiring innovative drug discovery. In addition, some natural products have been applied in clinical practice for infection, cancer, and autoimmunity over thousands of years and their promising curative effects and safety have been well-accepted. However, whether these natural products are primarily targeting type I IFN signaling and specific molecular targets involved are not fully elucidated. In the current review, we thoroughly summarize recent advances in the pharmacology researches of natural products for their type I IFN activity, including both agonism/activation and antagonism/inhibition, and their potential application as therapies. Furthermore, the source and chemical nature of natural products with type I IFN activity are highlighted and their specific molecular targets in the type I IFN pathway and mode of action are classified. In conclusion, natural products possessing type I IFN activity represent promising therapeutic strategies and have a bright prospect in the treatment of infection, cancer, and autoimmune diseases.

Changes and significance of type 2 innate lymphoid cells and their related factors in bronchopulmonary dysplasia / 中国当代儿科杂志

OBJECTIVES@#To investigate the changes and significance of type 2 innate lymphoid cells (ILC2), interleukin-33 (IL-33), interleukin-25 (IL-25), thymic stromal lymphopoietin (TSLP), interleukin-5 (IL-5), and interleukin-13 (IL-13) in peripheral blood of preterm infants with bronchopulmonary dysplasia (BPD).@*METHODS@#A total of 76 preterm infants with a gestational age of <32 weeks and a length of hospital stay of ≥14 days who were admitted to the Department of Pediatrics of the Affiliated Hospital of Jiangsu University from September 2020 to December 2021 were enrolled. According to the diagnostic criteria for BPD, they were divided into a BPD group with 30 infants and a non-BPD group with 46 infants. The two groups were compared in terms of the percentage of ILC2 and the levels of IL-33, IL-25, TSLP, IL-5, and IL-13 in peripheral blood on days 1, 7, and 14 after birth.@*RESULTS@#The BPD group had significantly lower birth weight and gestational age than the non-BPD group (P<0.05). On days 7 and 14 after birth, the BPD group had significantly higher levels of ILC2, IL-33, TSLP, and IL-5 than the non-BPD group (P<0.05), and these indices had an area under the curve of >0.7 in predicting the devolpment of BPD (P<0.05). Multivariate logistic regression analysis showed that after adjusting for gestational age and birth weight, peripheral blood IL-33, TSLP and IL-5 on days 7 and 14 after birth were closely related to the devolpment of BPD (P<0.05).@*CONCLUSIONS@#Early innate immune activation and upregulated expression of related factors may be observed in preterm infants with BPD. ILC2, IL-33, TSLP, and IL-5 may be used as biological indicators for early diagnosis of BPD.

Research progress on the role of type II innate lymphoid cells in liver diseases / 中华肝脏病杂志

Type II innate lymphoid cell (ILC2) is a newly identified innate immunological cell that belongs to the lymphocyte lineage in cell morphology, resides in the body's mucosal tissues, and has the dual functions of innate and adaptive immunity to promote tissue remodeling and repair after injury. Additionally, it is involved in the occurrence and development of a variety of liver diseases and plays an important role in maintaining the immunological homeostasis of the liver region. This article reviews the differentiation, development, and biological functions of ILC2, with particular attention to the research progress in liver diseases.

Research progress in immunology of DNA-dependent activator of IFN-regulatory factors (DAI) as a pattern recognition receptor / 细胞与分子免疫学杂志

DNA sensor, a kind of pattern recognition receptor (PRR), is widely expressed in innate immune cells. It activates the inflammatory signaling pathways and triggers an innate immune response by recognizing the pathogens or DNA in abnormal host cells. DNA-dependent activator of IFN-regulatory factors (DAI) is the first cytoplasmic DNA receptor discovered, which plays an important role in regulating the innate immune responses characterized by induction of interferon and programmed cell death. The article summarizes the molecular characteristics of DAI, its downstream signaling pathways, and its role and mechanism in anti-infective immunity, tumor immunity and inflammatory diseases. It also makes a preliminary exploration of the correlation between DAI and transplantation immunology, and provides a new target for the therapy of various immune diseases.

CGRP inhibits proliferation, activation and cytokine secretion of group 2 innate lymphoid cells (ILC2) in peripheral blood from patients with allergic rhinitis / 细胞与分子免疫学杂志

Objective To investigate the effect of calcitonin gene-related peptide (CGRP) on the regulation of group 2 innate lymphoid cells (ILC2) in the peripheral blood of patients with allergic rhinitis (AR). Methods Peripheral blood mononuclear cells (PBMCs) were extracted from normal healthy individuals and AR patients, then stimulated with CGRP, interleukin 33 (IL-33) and CGRP combined with IL-33 for 3 days, with blank stimulus as control. The percentage of ILC2 in the four groups was measured by flow cytometry. After being sorted, ILC2 was given to CGRP, IL-33 and CGRP combined with IL-33 stimulation for 3 days, with blank stimulus as control. The percentage of IL-5 and IL-13 positive cells in ILC2 was detected by flow cytometry, and the levels of IL-5 and IL-13 in ILC2 supernatant were measured by ELISA. Results The percentage of ILC2 in the peripheral blood of AR patients was significantly higher than that of the control group. The levels of IL-5+ILC2 and IL-13+ILC2 were significantly increased by IL-33 single stimulation after culturing PBMCs. After adding IL-33 combined with CGRP stimulation, the levels of IL-5+ILC2 and IL-13+ILC2 in PBMCs were significantly reduced; after CGRP single stimulation, the levels of IL-5+ILC2 and IL-13+ILC2 in PBMCs were further decreased. After ILC2 was sorted and cultured, the levels of IL-5+ILC2 and IL-13+ILC2 showed significant increase after IL-33 single stimulation. The levels of IL-5+ILC2 and IL-13+ILC2 were decreased by IL-33 and CGRP co-stimulation, and they were further reduced after CGRP single stimulation. Compared to IL-33 single stimulation, IL-5 and IL-13 levels dropped significantly due to the IL-33 and CGRP co-stimulation. The levels of IL-5 and IL-13 were further reduced by CGRP single stimulation. Conclusion CGRP inhibits the proliferation and activation of peripheral blood ILC2 in AR and exert anti-inflammatory effects in AR.

Imbalance of lymphoid cells in peripheral blood maintains the immunosuppression and promotes the development of lung adenocarcinoma / 细胞与分子免疫学杂志

Objectives Objectives To investigate how the imbalance of innate lymphoid cells (ILCs)in the peripheral blood of patients with lung adenocarcinoma affects the balance of downstream mononuclear macrophages and T helper (Th) cells, and to identify the impact of the imbalance of ILCs on the immune status and prognosis of lung adenocarcinoma. Methods The peripheral blood of 20 patients with lung adenocarcinoma and normal controls were collected. The percentage of ILCs, mononuclear macrophages and T lymphocyte in peripheral blood were analyzed by flow cytometry. The characteristic cytokine secretion levels of various types of immune cells in peripheral blood were detected by real-time fluorescence quantitative PCR. Results Compared with the normal controls, the proportion of M2 mononuclear macrophages, ILC1 and ILC2 in patients with lung adenocarcinoma was up-regulated, while the proportion of M1 mononuclear macrophages, CD4+ T and CD8+ T was down-regulated. The mRNA expression of related cytokines of M1 mononuclear macrophages and ILC1 were decreased; while the mRNA expression of related cytokines of M2 mononuclear macrophages and ILC2 were increased. Along with the decreased CD4+T cells-associated cytokine T-bet mRNA expression, and the increased GATA3 mRNA expression. Moreover, the expression of PD-1 in CD8+ T cells was also up-regulated. Conclusion The imbalance of ILCs in peripheral blood of patients with lung adenocarcinoma promotes the imbalance of mononuclear macrophages and Th cells, which altogether maintains the immunosuppression in patients with lung adenocarcinoma, and promotes the development of lung adenocarcinoma.

Role of innate immunity in the pathogenesis of ventilation-induced lung injury / 中华危重病急救医学

For patients receiving mechanical ventilation, mechanical ventilation is also an injury factor at the same time of treatment, which can lead to or aggravate lung injury, that is, ventilator-induced lung injury (VILI). The typical feature of VILI is that the mechanical stress is transmitted to cells through the pathway, leading to uncontrollable inflammatory cascade reaction, which causes the activation of inflammatory cells in the lung and the release of a large number of cytokines and inflammatory mediators. Among them, innate immunity is also involved in the occurrence and development of VILI. A large number of studies have shown that damaged lung tissue in VILI can regulate inflammatory response by releasing a large number of damage associated molecular pattern (DAMP). Pattern recognition receptor (PRR) participates in the activation of immune response by combining with DAMP, and releases a large number of inflammatory mediators to promote the occurrence and development of VILI. Recent studies have shown that inhibition of DAMP/PRR signaling pathway can play a protective role in VILI. Therefore, this article will mainly discuss the potential role of blocking DAMP/PRR signal pathway in VILI, and provide new ideas for the treatment of VILI.

Composite Sophora Colon-Soluble Capsule Ameliorates DSS-Induced Ulcerative Colitis in Mice via Gut Microbiota-Derived Butyric Acid and NCR+ ILC3 / 中国结合医学杂志

OBJECTIVE@#To investigate the effects of composite Sophora colon-soluble Capsule (CSCC) on gut microbiota-mediated short-chain fatty acids (SCFAs) production and downstream group 3 innate lymphoid cells (ILC3s) of dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) mice model.@*METHODS@#The main components of CSCC were analyzed by hybrid ultra-high-performance liquid chromatography ion mobility spectromety quadrupole time-of-flight mass spectrometry (UHPLC-IM-QTOF/MS). Twenty-four male BALB/c mice were randomly divided into 4 groups (n=6) by using a computer algorithm-generated random digital, including control, DSS model, mesalazine, and CSCC groups. A DSS-induced colitis mice model was established to determine the effects of CSCC by recording colonic weight, colonic length, index of colonic weight, and histological colonic score. The variations in ILC3s were assessed by immunofluorescence and flow cytometry. The results of gut microbiota and SCFAs were acquired by 16s rDNA and gas chromatography-mass spectrometry (GC-MS) analysis. The expression levels of NCR+ ILC3-, CCR6+ Nkp46- (Lti) ILC3-, and ILCreg-specific markers were detected by enzyme-linked immunosorbent assay, and real-time quantitative polymerase chain reaction and Western blot, respectively.@*RESULTS@#The main components of CSCC were matrine, ammothamnine, Sophora flavescens neoalcohol J, and Sophora oxytol U. After 7 days of treatment, CSCC significantly alleviated colitis by promoting the reproduction of intestinal probiotics manifested as upregulation of the abundance of Bacteroidetes species and specifically the Bacteroidales_S24-7 genus (P<0.05). Among the SCFAs, the content of butyric acid increased the most after CSCC treatment. Meanwhile, compared with the model group, Lti ILC3s and its biomarkers were significantly downregulated and NCR+ ILC3s were significantly elevated in the CSCC group (P<0.01). Further experiments revealed that ILC3s were differentiated from Lti ILC3s to NCR+ ILC3s, resulting in interleukin-22 production which regulates gut epithelial barrier function.@*CONCLUSION@#CSCC may exert a therapeutic effect on UC by improving the gut microbiota, promoting metabolite butyric acid production, and managing the ratio between NCR+ ILC3s and Lti ILC3s.

Mecanismos inmunológicos en Cnidaria: un sistema inmune basal de gran complejidad e interés bioprospectivo / Immunological mechanisms in Cnidaria: A highly complex basal immune system with bioprospective interest

Introducción: La protección ante agentes biológicos propios y externos de los cnidarios dependen de la inmunidad innata, la cual consta de tres procesos inmunológicos principales: 1) reconocimiento inmunológico, 2) señalización intracelular, y 3) respuesta efectora. Objetivo: Revisar críticamente el conocimiento actual del repertorio molecular involucrado en la respuesta inmune en cnidarios, así como, su papel en el establecimiento de la simbiosis, y las posibles aplicaciones biotecnológicas de las moléculas involucradas en el proceso de inmunidad. Métodos: Se realizó una revisión de artículos científicos encontrados a través de las bases de datos del NCBI, Google Scholar y Scielo, con palabras claves como inmunidad y/o reconocimiento inmunológico en cnidarios, en una ventana de tiempo de la última década, sin descartar literatura clásica más antigua. Resultados: El reconocimiento inmunológico consiste en receptores inmunológicos que reconocen patrones moleculares e inducen respuestas efectoras como la movilización de moléculas al sitio de la infección, la ingestión microbiana y la formación de moléculas que activan cascadas de señalización. La fase de señalización involucra mediadores de la traducción de señales que activan genes de trascripción, y cascadas de señalización intracelular que inician respuestas de defensa adecuadas. Las respuestas efectoras incluyen la capa superficial del mucus, péptidos antimicrobianos, especies reactivas de oxígeno y la respuesta celular mediada por fagocitosis. Por último, se presenta un esquema y una tabla integral de las vías de respuesta inmune en los cnidario. Conclusiones: La inmunidad en Cnidaria está mediada por mecanismos de defensa complejos integrados por receptores de reconocimiento de patógenos, vías de señalización intracelular, células y moléculas efectoras encargadas de la eliminación del patógeno, y reconocimiento-aceptación de simbiontes. El estudio de compuestos activos del sistema inmune en Cnidaria ha sido poco explorado, sin embargo, el trabajo realizado con otros compuestos presentes en las toxinas de este filo, los sitúa como una fuente importante de moléculas antimicrobianas dignas de un análisis de bioprospección.

Introduction: Cnidarians depend on innate immunity for protection against both their own and external biological agents. It consists of three main immunological processes: 1) immune recognition, 2) intracellular signaling, and 3) effector response. Objective: To critically review current knowledge of the molecular repertoire involved in the immune response in cnidarians, its role in symbiosis, and possible biotechnological applications. Methods: We used keywords such as immunity, and immunological recognition in cnidarians, in the NCBI, Scielo and Google Scholar databases, for the last decade. Results: Cnidarian immune recognition consists of molecular pattern receptors and responses such as the mobilization of molecules to the site of infection, microbial ingestion, and the formation of molecules that activate signaling cascades. The signaling phase involves translation mediators that activate transcriptional genes and intracellular signaling cascades that initiate defenses. Effector responses include surface layer mucus, antimicrobial peptides, reactive oxygen species, and the cellular response mediated by phagocytosis. Conclusions: Immunity in Cnidaria is mediated by complex defense mechanisms composed of pathogen recognition receptors, intracellular signaling pathways, effector cells and molecules responsible for pathogen elimination, and recognition of symbionts. There is a potential for toxin compounds useful as antimicrobial molecules.

Trasplante pulmonar: una perspectiva desde la inmunología / Lung transplantation: a perspective from immunology

Resumen El trasplante pulmonar implica una serie de desafíos, que como lo ha demostrado la historia, no sólo depende de un adecuado desarrollo de técnicas quirúrgicas, sino también de la comprensión de una serie de complejas interacciones inmunológicas celulares y humorales que serán las responsables del tipo de respuesta (innata y/o adquirida) fisiológica y que pudiesen desencadenar las complicaciones asociadas al trasplante (rechazo hiperagudo, agudo o crónico). Cada una de las cuales tiene su potencial prevención y/o tratamiento. El poder conocer esta serie de respuestas, permite al clínico anticiparse a algunos de estos eventos y evitar de mejor forma el daño y las consecuencias que pueden producir en los casos de trasplante pulmonar.

Lung transplantation involves a series of challenges, which as history has shown, depends not only on an adequate development of surgical techniques, but also on the understanding of a series of complex cellular and humoral immunological interactions that will be responsible for the type of physiological response (innate - acquired) and that could trigger the complications associated with transplantation (hyperacute, acute or chronic rejection). Each of which has its potential prevention and treatment. Being able to know this series of responses, allows the clinician to anticipate some of these events and to avoid in a better way the damage and the consequences that can occur in cases of lung transplantation.

Epigenetic regulation of microglia-mediated innate immune memory and neurological diseases / 生理学报

Microglia have the ability to mediate innate immune memory and can be reprogrammed by primary stimuli to enhance or inhibit the immune response of microglia to secondary stimuli. Inflammatory stimulation is an important factor for microglia to mediate innate immune memory. Single or repeated stimulation can induce microglia to form different phenotypes. Microglia-mediated innate immune response is involved in the regulation of immune memory. Enhancer modification is a key pathway of microglia epigenetic regulation, and the H3K27ac enhancer marker is closely related to immune training. TGF-β1 mediates the interaction between IL-10 and IL-1β, thereby influencing the microglial phenotype. Microglia glycolysis activity is increased after immune training, and oxidative phosphorylation is associated with immune tolerance. Innate immune memory is closely associated with neurodegenerative diseases, brain tumors, brain damage and psychosis. Further study on the mechanism of microglia-mediated innate immune memory is helpful to understand the occurrence and development of central nervous system diseases and provide new options for the treatment of central nervous system diseases.