Brain, Behavior, and Immunity最新文献

{"title":"The effects of chronic fatigue and chronic stress on alterations in immune cell responses to acute psychosocial stress","authors":"Nida Ali ,&nbsp;Jana Strahler ,&nbsp;Urs M. Nater","doi":"10.1016/j.bbi.2024.10.013","DOIUrl":"10.1016/j.bbi.2024.10.013","url":null,"abstract":"<div><div>Fatigue is a common and debilitating symptom of a broad spectrum of diseases. Previous research has shown that individuals suffering from chronic forms of fatigue experience significantly more stress compared to healthy individuals, suggesting that stress is a potential pathophysiological factor in the onset and maintenance of chronic fatigue. Individually, chronic experiences of fatigue and stress have been associated with disruptions in adaptive immunity. However, how chronic fatigue and chronic stress together affect immune regulation is not fully understood. Here, we investigated the unique and combined contribution of chronic fatigue and chronic stress on immune cell redistribution in response to, and recovery from, acute psychosocial stress. Eighty women with high or low levels of chronic fatigue and varying levels of chronic stress were exposed to a psychosocial laboratory stressor. Blood samples were collected 10 min before and then at 10, 40, and 100 min after the end of stress. The main lymphocyte subpopulations (CD3+, CD3 + CD4+, CD3 + CD8+, CD16 + CD56+, and CD19 + cells) were enumerated via flow cytometry. Acute stress resulted in an increase in CD8 + and CD16+/CD56 + cells, a decline in CD4 + cells, and no effects on CD19 + B lymphocytes. Importantly, the magnitude of immune cell redistribution during stress reactivity (CD3+, CD4+, CD16+/CD56 + ) and recovery (CD3 + ) was contingent on fatigue and chronic stress levels of individuals. Notably, in contrast to low-fatigued individuals, who showed steeper changes in cell populations, increasing levels of chronic stress did not impact immune cell migration responses in high-fatigued individuals. Our findings demonstrate the compounded blunting effects of fatigue and chronic stress on adaptive immune functioning, highlighting a potential pathway for vulnerability and detrimental effects on long-term health.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 707-716"},"PeriodicalIF":8.8,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142458319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ancient viral DNA in the human genome linked to neurodegenerative diseases","authors":"Rodrigo R.R. Duarte ,&nbsp;Douglas F. Nixon ,&nbsp;Timothy R. Powell","doi":"10.1016/j.bbi.2024.10.020","DOIUrl":"10.1016/j.bbi.2024.10.020","url":null,"abstract":"<div><h3>Background</h3><div>Human endogenous retroviruses (HERVs) are sequences in the human genome that originated from infections with ancient retroviruses during our evolution. Previous studies have linked HERVs to neurodegenerative diseases, but defining their role in aetiology has been challenging. Here, we used a retrotranscriptome-wide association study (rTWAS) approach to assess the relationships between genetic risk for neurodegenerative diseases and HERV expression in the brain, calculated with genomic precision.</div></div><div><h3>Methods</h3><div>We analysed genetic association statistics pertaining to Alzheimer’s disease, amyotrophic lateral sclerosis, multiple sclerosis, and Parkinson’s disease, using HERV expression models calculated from 792 cortical samples. Robust risk factors were considered those that survived multiple testing correction in the primary analysis, which were also significant in conditional and joint analyses, and that had a posterior inclusion probability above 0.5 in fine-mapping analyses.</div></div><div><h3>Results</h3><div>The primary analysis identified 12 HERV expression signatures associated with neurodegenerative disease susceptibility. We found one HERV expression signature robustly associated with amyotrophic lateral sclerosis on chromosome 12q14 (MER61_12q14.2) and one robustly associated with multiple sclerosis on chromosome 1p36 (ERVLE_1p36.32a). A co-expression analysis suggested that these HERVs are involved in homophilic cell adhesion via plasma membrane adhesion molecules.</div></div><div><h3>Conclusions</h3><div>We found HERV expression profiles robustly associated with amyotrophic lateral sclerosis and multiple sclerosis susceptibility, highlighting novel risk mechanisms underlying neurodegenerative disease, and offering potential new targets for therapeutic intervention.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 765-770"},"PeriodicalIF":8.8,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142458331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Social isolation promotes tumor immune evasion via β2-adrenergic receptor","authors":"Xueqin Zhao ,&nbsp;Fei Li ,&nbsp;Chen Cheng ,&nbsp;Mingyue Bi ,&nbsp;Jing Li ,&nbsp;Jingjing Cong ,&nbsp;Xuefu Wang","doi":"10.1016/j.bbi.2024.10.012","DOIUrl":"10.1016/j.bbi.2024.10.012","url":null,"abstract":"<div><div>Social isolation is a recognized risk factor for tumor initiation and mortality, but the role and mechanisms responsible for social isolation on tumor progression are poorly understood. In this study, we found that social isolation contributed to accelerated tumor growth and induced a remodeling of the tumor immune microenvironment, resulting in immunosuppression. Mechanistically, social isolation triggered the activation of the sympathetic nervous system, leading to impaired CD8⁺ T cell antitumor immune responses by activating β-adrenergic receptor 2 (β2-AR), which highly expressed on tumor-infiltrating CD8⁺ T cells. Pharmacological inhibition of β2-AR signaling effectively enhanced CD8⁺ T cell anti-tumor immune responses and improved the efficacy of anti-PD-1 immunotherapy in the context of social isolation. Thus, our study uncovers a mechanism through which social isolation induces tumor immune evasion and offers potential directions for cancer immunotherapy in socially isolated patients.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 607-618"},"PeriodicalIF":8.8,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142442408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CSF and blood signatures support classification of limbic encephalitis subtypes","authors":"Andreas Schulte-Mecklenbeck ,&nbsp;Andre Dik ,&nbsp;Christine Strippel ,&nbsp;Laura Bierhansl ,&nbsp;Niklas Meyer ,&nbsp;Lisanne Korn ,&nbsp;Matthias Pawlowski ,&nbsp;Saskia Räuber ,&nbsp;Judith Alferink ,&nbsp;Sven G Meuth ,&nbsp;Nico Melzer ,&nbsp;Gerd Meyer zu Hörste ,&nbsp;Harald Prüß ,&nbsp;Heinz Wiendl ,&nbsp;Catharina C. Gross ,&nbsp;Stjepana Kovac","doi":"10.1016/j.bbi.2024.10.018","DOIUrl":"10.1016/j.bbi.2024.10.018","url":null,"abstract":"<div><div>Autoimmune limbic encephalitis (ALE) represents a heterogeneous disease associated with antibodies targeting extracellular (ALE_extra) epitopes, intracellular (ALE_intra) epitopes, anti-glutamic acid decarboxylase65 ALE (ALE_GAD65), and ALE without detectable antibodies (ALE_abneg). Combining analysis of cellular parameters, investigated by flow cytometry, and soluble parameters in the blood and cerebrospinal fluid (CSF) from a large cohort of 148 ALE patients (33 ALE_extra, 12 ALE_intra, 28 ALE-GAD65, 37 ALE_abneg) in comparison to paradigmatic examples for neuro-inflammatory (51 relapsing remitting MS patients (RRMS)), and neuro-degenerative (34 Alzheimer’s disease patients (AD)) diseases revealed discrete immune signatures in ALE subgroups. Identification of ALE-subtype specific markers facilitated classification of rare ALE-associated tumors, which may prompt further diagnostic efforts in clinical practice. While ALE_intra exhibited features of neuro-inflammation, ALE_extra displayed features of neuro-inflammation as well as neuro-degeneration. Moreover, ALE_GAD65 and ALE_abneg lacked hallmarks of inflammation. This may explain the low efficacy of anti-inflammatory treatment regimens in ALE_GAD65 and presumably also ALE_abneg.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 697-706"},"PeriodicalIF":8.8,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142458321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicles from L. paracasei improve neuroinflammation, GABA neurotransmission and motor incoordination in hyperammonemic rats","authors":"Yaiza M. Arenas ,&nbsp;Gaspar Pérez-Martinez ,&nbsp;Carmina Montoliu ,&nbsp;Marta Llansola ,&nbsp;Vicente Felipo","doi":"10.1016/j.bbi.2024.10.002","DOIUrl":"10.1016/j.bbi.2024.10.002","url":null,"abstract":"<div><div>Patients with liver cirrhosis may show minimal hepatic encephalopathy (MHE) with motor incoordination and cognitive impairment that reduce life quality and span. Motor incoordination is due to neuroinflammation and enhanced GABAergic neurotransmission in cerebellum. Recent reports support that probiotics, including <em>L. casei</em>, may improve cognitive function in different pathologies and MHE in cirrhotic patients. Extracellular vesicles (EV) are small cell-derived membrane vesicles that carry bioactive molecules released from cells, including bacteria. We hypothesized that EV from <em>Lacticaseibacillus paracasei</em> (LC-EV) could improve neuroinflammation, GABAergic neurotransmission and motor function in MHE. We show that LC-EV treatment reverses glial activation and neuroinflammation in cerebellum and restore motor coordination in hyperammonemic rats. Moreover, ex vivo treatment of cerebellar slices from hyperammonemic rats with LC-EV also reverses glial activation and neuroinflammation, and the enhancement of the TNFR1-S1PR2-BDNF-TrkB and TNFR1-TrkB-pAKT-NFκB-glutaminase-GAT3 pathway<strong>s</strong> and of GABAergic neurotransmission. The results reported support that LC-EV may be used as a therapeutic tool to improve motor incoordination in patients with MHE.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 556-570"},"PeriodicalIF":8.8,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A critical analysis of stress-related gene regulation in isolated and connected individuals","authors":"Rizky Andana Pohan ,&nbsp;Ririn Dwi Astuti ,&nbsp;Putri Bunga Aisyah Pohan ,&nbsp;Marimbun Marimbun ,&nbsp;Wan Chalidaziah ,&nbsp;Nengsih Nengsih","doi":"10.1016/j.bbi.2024.09.035","DOIUrl":"10.1016/j.bbi.2024.09.035","url":null,"abstract":"<div><div>This letter responds to the article by Yvonne S. Yang et al. (2024) on the relationship between social isolation, loneliness, and stress-related gene expression, published in Brain, Behavior, and Immunity. The authors’ recruitment methods and use of genome-wide transcriptional profiling to assess the Conserved Transcriptional Response to Adversity (CTRA) are highly commendable, offering a comprehensive understanding of how social isolation impacts immune gene expression. However, we raise concerns about the small sample size, demographic limitations, cross-sectional design, and lack of correction for multiple comparisons, which may affect the study’s generalizability and validity. Despite these limitations, the study provides valuable insights, paving the way for future research to explore the complex interactions between social isolation, loneliness, and health. We recommend that future studies address these limitations to enhance the robustness of findings and the development of effective interventions.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 500-501"},"PeriodicalIF":8.8,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic treatment with the antipsychotic lurasidone modulates the neuroinflammatory changes associated with the vulnerability to chronic mild stress exposure in female rats","authors":"Veronica Begni ,&nbsp;Diana Morena Silipo ,&nbsp;Chiara Bottanelli ,&nbsp;Mariusz Papp ,&nbsp;Annamaria Cattaneo ,&nbsp;Marco Andrea Riva","doi":"10.1016/j.bbi.2024.10.001","DOIUrl":"10.1016/j.bbi.2024.10.001","url":null,"abstract":"<div><div>Stress exposure is a key risk factor for the development<!--> <!-->of depressive-like conditions. However, despite the higher incidence of Major Depressive Disorder in the female population, classical stress-based experimental paradigms have primarily focused on males. In the present study, we used the well-established chronic mild stress (CMS) paradigm to investigate the development of anhedonia, a cardinal symptom of affective disorders, in the female animals and we also studied the potential effect of the antipsychotic drug lurasidone in normalizing the alterations brought about by stress exposure. We found that three weeks of CMS exposure produced a significant reduction of sucrose intake in 50% of the animals (vulnerable, CMS-V), whereas the others were resilient (CMS-R). The development of an anhedonic phenotype in CMS-V was associated with a significant elevation of different immune markers, such as Complement C3 and C4, and inflammatory cytokines, including INFß and Il1ß in dorsal and ventral hippocampus. Interestingly, sub-chronic treatment with the antipsychotic drug lurasidone was able to revert the anhedonic phenotype while normalizing most of the molecular alterations found in rats vulnerable to CMS exposure. This study extends the ability of lurasidone to normalize the anhedonic phenotype in CMS rats also to females. Moreover, we provide novel evidence on lurasidone’s potential effectiveness in treating mental disorders characterized by immune-inflammatory dysfunction.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 586-596"},"PeriodicalIF":8.8,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review of intravenous immunoglobulin in the treatment of neuroimmune conditions, acute COVID-19 infection, and post-acute sequelae of COVID-19 Syndrome","authors":"Brinkley A. Morse ,&nbsp;Katherine Motovilov ,&nbsp;W. Michael Brode ,&nbsp;Francis Michael Tee ,&nbsp;Esther Melamed","doi":"10.1016/j.bbi.2024.10.006","DOIUrl":"10.1016/j.bbi.2024.10.006","url":null,"abstract":"<div><div>Intravenous immunoglobulin (IVIG) is an immunomodulatory therapy that has been studied in several neuroimmune conditions, such as Guillain-Barré Syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and multiple sclerosis. It has also been proposed as a potential treatment option for acute COVID-19 infection and post-acute sequelae of SARS-CoV-2 infection (PASC). IVIG is thought to function by providing the recipient with a pool of antibodies, which can, in turn, modulate immune responses through multiple mechanisms including neutralization of cytokines and autoantibodies, saturation of neonatal fragment crystallizable receptors, inhibition of complement activation, and regulation of T and B cell mediated inflammation. In acute COVID-19, studies have shown that early administration of IVIG and plasmapheresis in severe cases can reduce the need for mechanical ventilation, shorten ICU and hospital stays, and lower mortality. Similarly, in PASC, while research is still in early stages, IVIG has been shown to alleviate persistent symptoms in small patient cohorts. Furthermore, IVIG has shown benefits in another condition which has symptomatic overlap with PASC, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), though studies have yielded mixed results. It is important to note that IVIG can be associated with several potential adverse effects, such as anaphylaxis, headaches, thrombosis, liver enzyme elevations and renal complications. In addition, the high cost of IVIG can be a deterrent for payers and patients. This review provides a comprehensive update on the use of IVIG in multiple neuroimmune conditions, ME/CFS, acute COVID-19, and PASC, as well as covers its history, production, pricing, and mechanisms of action. We also identify key areas of future research, including the need to optimize the use of Ig product dosing, timing, and patient selection across conditions, particularly in the context of COVID-19 and PASC.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 725-738"},"PeriodicalIF":8.8,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deleterious effects of social isolation on neuroendocrine-immune status, and cancer progression in rats","authors":"Estherina Trachtenberg ,&nbsp;Keren Ruzal ,&nbsp;Elad Sandbank ,&nbsp;Einat Bigelman ,&nbsp;Itay Ricon-Becker ,&nbsp;Steve W. Cole ,&nbsp;Shamgar Ben-Eliyahu ,&nbsp;Inbal Ben-Ami Bartal","doi":"10.1016/j.bbi.2024.10.005","DOIUrl":"10.1016/j.bbi.2024.10.005","url":null,"abstract":"<div><div>Accumulating evidence indicates that social isolation (SI) in humans and rodents is associated with increased cancer incidence and mortality, yet mediating mechanisms remain elusive. Here, we examine the neuroendocrine and immunological consequences of SI and its short- and long-term physiological impacts in naïve and cancer-bearing rats. Findings indicate that isolated animals experienced a significant decrease in weight compared to controls. Specifically, females showed a marked weight decrease during the first week of isolation. Isolated rats had significantly higher numbers of MADB106 experimental pulmonary metastases. Although mortality rates were higher in isolated tumor-bearing rats, unexpectedly, they exhibited a reduced growth rate of orthotopically implanted MADB106 tumors. Transcriptomic analyses of these excised tumors indicated a major downregulation in the expression of various genes, including those associated with pro-metastatic processes (e.g., EMT). In naïve rats (no cancer), levels of IL-6 increased, and total IgG levels decreased under SI conditions. A mixed effect was found for TNFα, which increased in females and decreased in males. In the central nervous system, isolated rats showed altered gene expression in key brain regions associated with stress responses and social behavior. The paraventricular nucleus of the thalamus emerged as a significantly affected region, along with the bed nucleus of the stria terminalis. Changes were observed in the expression of oxytocin, serotonin, and dopamine receptors. Isolated rats also exhibited greater alterations in hypothalamic–pituitary–adrenal (HPA) axis-related regulation and an increase in plasma CORT levels. Our study highlights the profound impact of SI on metastatic processes. Additionally, the potential detrimental effects of SI on thermoregulation were discussed, emphasizing the importance of social thermoregulation in maintaining physiological stability and highlighting the need to avoid single-caging practices in research. We report neuro-immune interactions and changes in brain gene expression, highlighting the need for further research into these underlying processes to improve outcomes in animal models and potential interventions for cancer patients through increased social support.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"123 ","pages":"Pages 524-539"},"PeriodicalIF":8.8,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toward a better understanding of T cell dysregulation in autism: An integrative review.","authors":"R J Moreno, R Amara, P Ashwood","doi":"10.1016/j.bbi.2024.10.009","DOIUrl":"https://doi.org/10.1016/j.bbi.2024.10.009","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) is a highly heterogeneous disorder characterized by impairments in social, communicative, and restrictive behaviors. Over the past 20 years, research has highlighted the role of the immune system in regulating neurodevelopment and behavior. In ASD, immune abnormalities are frequently observed, such as elevations in pro-inflammatory cytokines, alterations in immune cell frequencies, and dysregulated mechanisms of immune suppression. The adaptive immune system - the branch of the immune system conferring cellular immunity - may be involved in the etiology of ASD. Specifically, dysregulated T cell activity, characterized by altered cellular function and increased cytokine release, presence of inflammatory phenotypes and altered cellular signaling, has been consistently observed in several studies across multiple laboratories and geographic regions. Similarly, mechanisms regulating their activation are also disrupted. T cells at homeostasis coordinate the healthy development of the central nervous system (CNS) during early prenatal and postnatal development, and aid in CNS maintenance into adulthood. Thus, T cell dysregulation may play a role in neurodevelopment and the behavioral and cognitive manifestations observed in ASD. Outside of the CNS, aberrant T cell activity may also be responsible for the increased frequency of immune based conditions in the ASD population, such as allergies, gut inflammation and autoimmunity. In this review, we will discuss the current understanding of T cell biology in ASD and speculate on mechanisms behind their dysregulation. This review also evaluates how aberrant T cell biology affects gastrointestinal issues and behavior in the context of ASD.</p>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":" ","pages":""},"PeriodicalIF":8.8,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}