The primary mechanism of secondary injury after cerebral ischemia may be the brain inflammation that emerges after an ischemic stroke,which promotes neuronal death and inhibits nerve tissue regeneration.As the first i...The primary mechanism of secondary injury after cerebral ischemia may be the brain inflammation that emerges after an ischemic stroke,which promotes neuronal death and inhibits nerve tissue regeneration.As the first immune cells to be activated after an ischemic stroke,microglia play an important immunomodulatory role in the progression of the condition.After an ischemic stroke,peripheral blood immune cells(mainly T cells)are recruited to the central nervous system by chemokines secreted by immune cells in the brain,where they interact with central nervous system cells(mainly microglia)to trigger a secondary neuroimmune response.This review summarizes the interactions between T cells and microglia in the immune-inflammatory processes of ischemic stroke.We found that,during ischemic stroke,T cells and microglia demonstrate a more pronounced synergistic effect.Th1,Th17,and M1 microglia can co-secrete proinflammatory factors,such as interferon-γ,tumor necrosis factor-α,and interleukin-1β,to promote neuroinflammation and exacerbate brain injury.Th2,Treg,and M2 microglia jointly secrete anti-inflammatory factors,such as interleukin-4,interleukin-10,and transforming growth factor-β,to inhibit the progression of neuroinflammation,as well as growth factors such as brain-derived neurotrophic factor to promote nerve regeneration and repair brain injury.Immune interactions between microglia and T cells influence the direction of the subsequent neuroinflammation,which in turn determines the prognosis of ischemic stroke patients.Clinical trials have been conducted on the ways to modulate the interactions between T cells and microglia toward anti-inflammatory communication using the immunosuppressant fingolimod or overdosing with Treg cells to promote neural tissue repair and reduce the damage caused by ischemic stroke.However,such studies have been relatively infrequent,and clinical experience is still insufficient.In summary,in ischemic stroke,T cell subsets and activated microglia act synergistically to regulate inflammatory progression,mainly by secreting inflammatory factors.In the future,a key research direction for ischemic stroke treatment could be rooted in the enhancement of anti-inflammatory factor secretion by promoting the generation of Th2 and Treg cells,along with the activation of M2-type microglia.These approaches may alleviate neuroinflammation and facilitate the repair of neural tissues.展开更多
Background:Xiaoqinglong decoction(XQLD)is a classic Chinese medicinal formula that is widely used to treat allergic asthma.Recently,the use of XQLD to treat allergic asthma has inspired research to determine its mecha...Background:Xiaoqinglong decoction(XQLD)is a classic Chinese medicinal formula that is widely used to treat allergic asthma.Recently,the use of XQLD to treat allergic asthma has inspired research to determine its mechanism of action.Because dendritic cells(DCs)and the T helper 1(Th1)/Th2 cytokine balance play important roles in allergic asthma,the present work aimed to assess how these immune system components are affected by XQLD.Methods:Thirty-six female BALB/C mice were randomly divided into three groups:an ovalbumin-based allergic asthma model group,a XQLD treatment group,and a control group.Histology was performed with haematoxylin and eosin staining and immunohistochemical staining.Bronchoalveolar lavage fluid and blood were collected from the animals and used to analyze the composition of inflammatory cells and expression levels of the cytokines interleukin(IL)-5 and IL-13.The thymic stromal lymphopoietin(TSLP)protein expression was assessed by western blot analysis,and the Gata3 and Tbx21 mRNA levels were assessed by polymerase chain reaction.Results:Compared with the OVA group,the levels of TSLP expression,IL-5,IL-13,and immunoglobulin E in the XQLD group were lower(all P<.01).The level of IL-4-expressing cells(Th2 cells)was lower(P=.0013),and the percentage of IFN-g-expressing cells(Th1 cells)was higher in the XQLD group compared with those in the OVA group(P=.0065).In addition,XQLD increased the expression of Tbx21 mRNA and decreased the expression of Gata3 mRNA in the lungs compared with the OVA group(both P<.01).Conclusion:These findings suggest that XQLD may ameliorate the course of allergic asthma by regulating the Gata3/Tbx21 balance and inhibiting TSLP expression,changes which are indicative of an altered Th1/Th2 balance.Thus,the clinical effectiveness of XQLD in treating allergic asthma may be due to its regulation of Th1/Th2 balance.展开更多
基金supported by the National Natural Science Foundation of China,Nos.82104560(to CL),U21A20400(to QW)the Natural Science Foundation of Beijing,No.7232279(to XW)the Project of Beijing University of Chinese Medicine,No.2022-JYB-JBZR-004(to XW)。
文摘The primary mechanism of secondary injury after cerebral ischemia may be the brain inflammation that emerges after an ischemic stroke,which promotes neuronal death and inhibits nerve tissue regeneration.As the first immune cells to be activated after an ischemic stroke,microglia play an important immunomodulatory role in the progression of the condition.After an ischemic stroke,peripheral blood immune cells(mainly T cells)are recruited to the central nervous system by chemokines secreted by immune cells in the brain,where they interact with central nervous system cells(mainly microglia)to trigger a secondary neuroimmune response.This review summarizes the interactions between T cells and microglia in the immune-inflammatory processes of ischemic stroke.We found that,during ischemic stroke,T cells and microglia demonstrate a more pronounced synergistic effect.Th1,Th17,and M1 microglia can co-secrete proinflammatory factors,such as interferon-γ,tumor necrosis factor-α,and interleukin-1β,to promote neuroinflammation and exacerbate brain injury.Th2,Treg,and M2 microglia jointly secrete anti-inflammatory factors,such as interleukin-4,interleukin-10,and transforming growth factor-β,to inhibit the progression of neuroinflammation,as well as growth factors such as brain-derived neurotrophic factor to promote nerve regeneration and repair brain injury.Immune interactions between microglia and T cells influence the direction of the subsequent neuroinflammation,which in turn determines the prognosis of ischemic stroke patients.Clinical trials have been conducted on the ways to modulate the interactions between T cells and microglia toward anti-inflammatory communication using the immunosuppressant fingolimod or overdosing with Treg cells to promote neural tissue repair and reduce the damage caused by ischemic stroke.However,such studies have been relatively infrequent,and clinical experience is still insufficient.In summary,in ischemic stroke,T cell subsets and activated microglia act synergistically to regulate inflammatory progression,mainly by secreting inflammatory factors.In the future,a key research direction for ischemic stroke treatment could be rooted in the enhancement of anti-inflammatory factor secretion by promoting the generation of Th2 and Treg cells,along with the activation of M2-type microglia.These approaches may alleviate neuroinflammation and facilitate the repair of neural tissues.
基金the National Natural Science Foundation of China(816015085).
文摘Background:Xiaoqinglong decoction(XQLD)is a classic Chinese medicinal formula that is widely used to treat allergic asthma.Recently,the use of XQLD to treat allergic asthma has inspired research to determine its mechanism of action.Because dendritic cells(DCs)and the T helper 1(Th1)/Th2 cytokine balance play important roles in allergic asthma,the present work aimed to assess how these immune system components are affected by XQLD.Methods:Thirty-six female BALB/C mice were randomly divided into three groups:an ovalbumin-based allergic asthma model group,a XQLD treatment group,and a control group.Histology was performed with haematoxylin and eosin staining and immunohistochemical staining.Bronchoalveolar lavage fluid and blood were collected from the animals and used to analyze the composition of inflammatory cells and expression levels of the cytokines interleukin(IL)-5 and IL-13.The thymic stromal lymphopoietin(TSLP)protein expression was assessed by western blot analysis,and the Gata3 and Tbx21 mRNA levels were assessed by polymerase chain reaction.Results:Compared with the OVA group,the levels of TSLP expression,IL-5,IL-13,and immunoglobulin E in the XQLD group were lower(all P<.01).The level of IL-4-expressing cells(Th2 cells)was lower(P=.0013),and the percentage of IFN-g-expressing cells(Th1 cells)was higher in the XQLD group compared with those in the OVA group(P=.0065).In addition,XQLD increased the expression of Tbx21 mRNA and decreased the expression of Gata3 mRNA in the lungs compared with the OVA group(both P<.01).Conclusion:These findings suggest that XQLD may ameliorate the course of allergic asthma by regulating the Gata3/Tbx21 balance and inhibiting TSLP expression,changes which are indicative of an altered Th1/Th2 balance.Thus,the clinical effectiveness of XQLD in treating allergic asthma may be due to its regulation of Th1/Th2 balance.
