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Editor | XI Autism spectrum disorder is a group of central nervous system developmental diseases with complex pathogenesis, highly heterogeneous etiology, and huge unmet clinical needs.
At present, the academic community is mainly focusing on its genetic etiology and pathological mechanism.
It has been found that part of the occurrence of autism can be attributed to hundreds of genetic abnormalities, so there is a lack of universal targets to support the development of conventional drugs.
The results of epidemiology and laboratory animal studies have shown that maternal immune activation (MIA) triggered by pathogens from the mother during pregnancy is an important risk factor for neuropsychiatric diseases such as autism in the offspring; at the same time, MIA has a peripheral and neuroimmune effect on offspring.
The system can have a lasting effect, which may be the cause of some immune abnormal autism.
On April 15, 2021, Professor Zhou Zikai from the Shanghai Mental Health Center-Shanghai Institute of Materia Medica of the Chinese Academy of Sciences and Professor Ji Minjun from the State Key Laboratory of Reproductive Medicine of Nanjing Medical University and Professor Ji Minjun from the Department of Pathogenic Biology published a report on Nature Neuroscience Research paper Rescue of maternal immune activation-induced behavioral abnormalities in adult mouse offspring by pathogen-activated maternal Treg cells.
The study established a new disease animal model of MIA (maternal immune activation), revealed the mechanism by which MIA affects the immune system of offspring and causes autism-related phenotypes, and found that it can be improved by regulating the immune system of adult offspring mice.
Autism phenotype.
The researchers first used the Toxoplasma gondii tachyzoite soluble antigen (STAg), which infects one third of the world’s population, to induce MIA to establish a mouse model with immune abnormalities and autism phenotypes in the offspring.
Compared with the two chemicals commonly used in academia, the virus mimic poly(I:C) and the bacterial mimic LPS, the parasite mimic STAg is a complex antigen, which can more comprehensively induce abnormal immune lineage, especially it can effectively induce acquisition Sexual cellular immune response.
The results found that: the offspring of sick mice have peripheral and neuroimmune spectrum abnormalities until adulthood, and their CD4+ T cell profile is highly consistent with some autistic patients; and sick mice have the core symptoms of autism such as social interaction defects, repetitive stereotypes, and communication disorders , And a significant anxiety phenotype.
After adoptive Treg cell transfer therapy in adult sick mice, the researchers found that although the improvement in the abnormal microstructure of white matter in the brain of sick mice was relatively limited, the treatment effectively reversed the extreme Partial immunological and behavioral phenotypes.
In addition, using single-cell sequencing technology (scRNA-seq) to compare the transcriptomes of Treg cells from different sources, the researchers identified a group of high-efficiency Treg cell subsets and their transcriptomic characteristics.
This type of high-efficiency Treg cells Can better move into the brain area associated with disease symptoms and take effect.
This work builds and studies a new MIA disease animal model with autism phenotype, and proposes that the use of regulatory T cell drugs engineered according to the molecular characteristics of the above-mentioned high-efficiency cell subsets is expected to improve the core of immune abnormal autism Symptoms provide new ideas for follow-up clinical translational research.
Xu Zhipeng, associate professor of Nanjing Medical University, Zhang Xiaoyun, postdoctoral fellow at the Shanghai Institute of Materia Medica, Chinese Academy of Sciences, and Chang Hao, a doctoral student at Nanjing Medical University, are the co-first authors.
Shanghai Institute of Materia Medica, Chinese Academy of Sciences/Mental Health Center Affiliated to Shanghai Jiao Tong University School of Medicine (concurrently) Researcher Zhou Zikai and Professor Ji Minjun from Nanjing Medical University are the co-corresponding authors.
Graphic abstract: MIA disease model with immune abnormal autism phenotype and the onset mechanism of adoptive Treg cell therapy.
Original link:Reprinting instructions [Non-original articles] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author owns all Legal rights, offenders must be investigated.
At present, the academic community is mainly focusing on its genetic etiology and pathological mechanism.
It has been found that part of the occurrence of autism can be attributed to hundreds of genetic abnormalities, so there is a lack of universal targets to support the development of conventional drugs.
The results of epidemiology and laboratory animal studies have shown that maternal immune activation (MIA) triggered by pathogens from the mother during pregnancy is an important risk factor for neuropsychiatric diseases such as autism in the offspring; at the same time, MIA has a peripheral and neuroimmune effect on offspring.
The system can have a lasting effect, which may be the cause of some immune abnormal autism.
On April 15, 2021, Professor Zhou Zikai from the Shanghai Mental Health Center-Shanghai Institute of Materia Medica of the Chinese Academy of Sciences and Professor Ji Minjun from the State Key Laboratory of Reproductive Medicine of Nanjing Medical University and Professor Ji Minjun from the Department of Pathogenic Biology published a report on Nature Neuroscience Research paper Rescue of maternal immune activation-induced behavioral abnormalities in adult mouse offspring by pathogen-activated maternal Treg cells.
The study established a new disease animal model of MIA (maternal immune activation), revealed the mechanism by which MIA affects the immune system of offspring and causes autism-related phenotypes, and found that it can be improved by regulating the immune system of adult offspring mice.
Autism phenotype.
The researchers first used the Toxoplasma gondii tachyzoite soluble antigen (STAg), which infects one third of the world’s population, to induce MIA to establish a mouse model with immune abnormalities and autism phenotypes in the offspring.
Compared with the two chemicals commonly used in academia, the virus mimic poly(I:C) and the bacterial mimic LPS, the parasite mimic STAg is a complex antigen, which can more comprehensively induce abnormal immune lineage, especially it can effectively induce acquisition Sexual cellular immune response.
The results found that: the offspring of sick mice have peripheral and neuroimmune spectrum abnormalities until adulthood, and their CD4+ T cell profile is highly consistent with some autistic patients; and sick mice have the core symptoms of autism such as social interaction defects, repetitive stereotypes, and communication disorders , And a significant anxiety phenotype.
After adoptive Treg cell transfer therapy in adult sick mice, the researchers found that although the improvement in the abnormal microstructure of white matter in the brain of sick mice was relatively limited, the treatment effectively reversed the extreme Partial immunological and behavioral phenotypes.
In addition, using single-cell sequencing technology (scRNA-seq) to compare the transcriptomes of Treg cells from different sources, the researchers identified a group of high-efficiency Treg cell subsets and their transcriptomic characteristics.
This type of high-efficiency Treg cells Can better move into the brain area associated with disease symptoms and take effect.
This work builds and studies a new MIA disease animal model with autism phenotype, and proposes that the use of regulatory T cell drugs engineered according to the molecular characteristics of the above-mentioned high-efficiency cell subsets is expected to improve the core of immune abnormal autism Symptoms provide new ideas for follow-up clinical translational research.
Xu Zhipeng, associate professor of Nanjing Medical University, Zhang Xiaoyun, postdoctoral fellow at the Shanghai Institute of Materia Medica, Chinese Academy of Sciences, and Chang Hao, a doctoral student at Nanjing Medical University, are the co-first authors.
Shanghai Institute of Materia Medica, Chinese Academy of Sciences/Mental Health Center Affiliated to Shanghai Jiao Tong University School of Medicine (concurrently) Researcher Zhou Zikai and Professor Ji Minjun from Nanjing Medical University are the co-corresponding authors.
Graphic abstract: MIA disease model with immune abnormal autism phenotype and the onset mechanism of adoptive Treg cell therapy.
Original link:Reprinting instructions [Non-original articles] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author owns all Legal rights, offenders must be investigated.
