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Research Review: The role of cytokines in depression in adolescents: a systematic review / Natalie T. MILLS in Journal of Child Psychology and Psychiatry, 54-8 (August 2013)
[article]
Titre : Research Review: The role of cytokines in depression in adolescents: a systematic review Type de document : Texte imprimé et/ou numérique Auteurs : Natalie T. MILLS, Auteur ; James G. SCOTT, Auteur ; Naomi R. WRAY, Auteur ; Sarah COHEN-WOODS, Auteur ; BERNHARD T. BAUNE, Auteur Article en page(s) : p.816-835 Langues : Anglais (eng) Mots-clés : Cytokines inflammation immune system MDD cognition stress Index. décimale : PER Périodiques Résumé : Background While cytokines have been implicated in the pathophysiology of depression in adults, the potential role in younger age groups such as adolescents is less clear. This article therefore reviews the literature (a) to explore the relationship between cytokines and depression in adolescents, and (b) to examine how cytokines may be related to adolescent depression in the context of other neurobiological theories of depression. Method A systematic review of the scientific literature on the subject was conducted in February 2013, searching the Web of Knowledge, PubMed (Medline), PsycInfo and Cochrane electronic databases. Results Eighteen studies were identified measuring both depression or depressive symptoms and cytokines or immune markers in adolescents. Adolescents with depression show age-specific characteristics of the immune and inflammatory system, specifically in NK cell activity and in pro-inflammatory cytokines (such as IL-1? and TNF-?). In addition, the role of cytokines in adolescent depression is influenced by neurodevelopment, hormonal changes, stress and trauma. Conclusions There may be differences in the neurobiology of adolescent major depressive disorder (MDD) compared with adult MDD. Increased understanding of the role of cytokines in adolescent MDD may lead to improved outcomes in the treatment of adolescent depression. En ligne : http://dx.doi.org/10.1111/jcpp.12080 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=210
in Journal of Child Psychology and Psychiatry > 54-8 (August 2013) . - p.816-835[article] Research Review: The role of cytokines in depression in adolescents: a systematic review [Texte imprimé et/ou numérique] / Natalie T. MILLS, Auteur ; James G. SCOTT, Auteur ; Naomi R. WRAY, Auteur ; Sarah COHEN-WOODS, Auteur ; BERNHARD T. BAUNE, Auteur . - p.816-835.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 54-8 (August 2013) . - p.816-835
Mots-clés : Cytokines inflammation immune system MDD cognition stress Index. décimale : PER Périodiques Résumé : Background While cytokines have been implicated in the pathophysiology of depression in adults, the potential role in younger age groups such as adolescents is less clear. This article therefore reviews the literature (a) to explore the relationship between cytokines and depression in adolescents, and (b) to examine how cytokines may be related to adolescent depression in the context of other neurobiological theories of depression. Method A systematic review of the scientific literature on the subject was conducted in February 2013, searching the Web of Knowledge, PubMed (Medline), PsycInfo and Cochrane electronic databases. Results Eighteen studies were identified measuring both depression or depressive symptoms and cytokines or immune markers in adolescents. Adolescents with depression show age-specific characteristics of the immune and inflammatory system, specifically in NK cell activity and in pro-inflammatory cytokines (such as IL-1? and TNF-?). In addition, the role of cytokines in adolescent depression is influenced by neurodevelopment, hormonal changes, stress and trauma. Conclusions There may be differences in the neurobiology of adolescent major depressive disorder (MDD) compared with adult MDD. Increased understanding of the role of cytokines in adolescent MDD may lead to improved outcomes in the treatment of adolescent depression. En ligne : http://dx.doi.org/10.1111/jcpp.12080 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=210 Altered Peripheral and Central Inflammatory Responses in a Mouse Model of Autism / Luciana LUCCHINA in Autism Research, 7-2 (April 2014)
[article]
Titre : Altered Peripheral and Central Inflammatory Responses in a Mouse Model of Autism Type de document : Texte imprimé et/ou numérique Auteurs : Luciana LUCCHINA, Auteur ; Amaicha Mara DEPINO, Auteur Article en page(s) : p.273-289 Mots-clés : valproic acid cytokines microglia astroglia hypothalamus–pituitary–adrenal axis behavior Index. décimale : PER Périodiques Résumé : Increasing clinical and experimental evidence links immune and inflammatory alterations with the pathogenesis of autism spectrum disorders (ASD). Autistic individuals show signs of neuroinflammation, altered inflammatory responses, and immune abnormalities throughout life. Mice injected subcutaneously with 600?mg/kg valproic acid (VPA600) at gestational day 12.5 show reduced social interaction in adulthood (at 8 weeks of age), and they have been proposed as a mouse model of autism. Here, we show that these adult animals present signs of chronic glial activation in the hippocampus and the cerebellum. Moreover, when they are challenged with a peripheral inflammatory stimulus (intraperitoneal lipopolysaccharides, LPS), VPA600 animals show an exacerbated inflammatory response. Two hours after LPS injection, VPA600 animals secrete more corticosterone to the blood than control mice, and show an increase in the levels of expression of proinflammatory cytokines in the spleen. After LPS challenge, VPA600 mice also show signs of increased neuroinflammation compared with control mice: they have more microglial cells in the hippocampus, and they show higher levels of proinflammatory cytokines in the cerebellum. Our results provide evidence of basal neuroinflammation and an altered inflammatory response in the VPA model of autism. We propose that this model can be used to evaluate the contribution of inflammatory reactivity to autism-related behaviors. These studies will contribute to elucidate the role of the inflammatory alterations observed in ASD individuals. En ligne : http://dx.doi.org/10.1002/aur.1338 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=230
in Autism Research > 7-2 (April 2014) . - p.273-289[article] Altered Peripheral and Central Inflammatory Responses in a Mouse Model of Autism [Texte imprimé et/ou numérique] / Luciana LUCCHINA, Auteur ; Amaicha Mara DEPINO, Auteur . - p.273-289.
in Autism Research > 7-2 (April 2014) . - p.273-289
Mots-clés : valproic acid cytokines microglia astroglia hypothalamus–pituitary–adrenal axis behavior Index. décimale : PER Périodiques Résumé : Increasing clinical and experimental evidence links immune and inflammatory alterations with the pathogenesis of autism spectrum disorders (ASD). Autistic individuals show signs of neuroinflammation, altered inflammatory responses, and immune abnormalities throughout life. Mice injected subcutaneously with 600?mg/kg valproic acid (VPA600) at gestational day 12.5 show reduced social interaction in adulthood (at 8 weeks of age), and they have been proposed as a mouse model of autism. Here, we show that these adult animals present signs of chronic glial activation in the hippocampus and the cerebellum. Moreover, when they are challenged with a peripheral inflammatory stimulus (intraperitoneal lipopolysaccharides, LPS), VPA600 animals show an exacerbated inflammatory response. Two hours after LPS injection, VPA600 animals secrete more corticosterone to the blood than control mice, and show an increase in the levels of expression of proinflammatory cytokines in the spleen. After LPS challenge, VPA600 mice also show signs of increased neuroinflammation compared with control mice: they have more microglial cells in the hippocampus, and they show higher levels of proinflammatory cytokines in the cerebellum. Our results provide evidence of basal neuroinflammation and an altered inflammatory response in the VPA model of autism. We propose that this model can be used to evaluate the contribution of inflammatory reactivity to autism-related behaviors. These studies will contribute to elucidate the role of the inflammatory alterations observed in ASD individuals. En ligne : http://dx.doi.org/10.1002/aur.1338 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=230 Neuroinflammatory Gene Expression Alterations in Anterior Cingulate Cortical White and Gray Matter of Males With Autism Spectrum Disorder / Aubrey N. SCIARA in Autism Research, 13-6 (June 2020)
[article]
Titre : Neuroinflammatory Gene Expression Alterations in Anterior Cingulate Cortical White and Gray Matter of Males With Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Aubrey N. SCIARA, Auteur ; Brooke BEASLEY, Auteur ; Jessica D. CRAWFORD, Auteur ; Emma P. ANDERSON, Auteur ; Tiffani CARRASCO, Auteur ; Shimin ZHENG, Auteur ; Gregory A. ORDWAY, Auteur ; Michelle J. CHANDLEY, Auteur Article en page(s) : p.870-884 Langues : Anglais (eng) Mots-clés : autism cytokines neuroinflammation pathology postmortem white matter Index. décimale : PER Périodiques Résumé : Evidence for putative pathophysiological mechanisms of autism spectrum disorder (ASD), including peripheral inflammation, blood-brain barrier disruption, white matter alterations, and abnormal synaptic overgrowth, indicate a possible involvement of neuroinflammation in the disorder. Neuroinflammation plays a role in the development and maintenance of the dendritic spines involved in glutamatergic and GABAergic neurotransmission, and also influences blood-brain permeability. Cytokines released from microglia can impact the length, location or organization of dendritic spines on excitatory and inhibitory cells as well as recruit and impact glial cell function around the neurons. In this study, gene expression levels of anti- and pro-inflammatory signaling molecules, as well as oligodendrocyte and astrocyte marker proteins, were measured in both gray and white matter tissue in the anterior cingulate cortex from ASD and age-matched typically developing (TD) control brain donors, ranging from ages 4 to 37?years. Expression levels of the pro-inflammatory gene, HLA-DR, were significantly reduced in gray matter and expression levels of the anti-inflammatory gene MRC1 were significantly elevated in white matter from ASD donors as compared to TD donors, but neither retained statistical significance after correction for multiple comparisons. Modest trends toward differences in expression levels were also observed for the pro-inflammatory (CD68, IL1?) and anti-inflammatory genes (IGF1, IGF1R) comparing ASD donors to TD donors. The direction of gene expression changes comparing ASD to TD donors did not reveal consistent findings implicating an elevated pro- or anti-inflammatory state in ASD. However, altered expression of pro- and anti-inflammatory gene expression indicates some involvement of neuroinflammation in ASD. Autism Res 2020, 13: 870-884. © 2020 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: The anterior cingulate cortex is an integral brain region in modulating social behaviors including nonverbal communication. The study found that inflammatory gene expression levels were altered in this brain region. We hypothesize that the inflammatory changes in this area could impact neuronal function. The finding has future implications in using these molecular markers to identify potential environmental exposures and distinct cell differences in autism. En ligne : http://dx.doi.org/10.1002/aur.2284 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427
in Autism Research > 13-6 (June 2020) . - p.870-884[article] Neuroinflammatory Gene Expression Alterations in Anterior Cingulate Cortical White and Gray Matter of Males With Autism Spectrum Disorder [Texte imprimé et/ou numérique] / Aubrey N. SCIARA, Auteur ; Brooke BEASLEY, Auteur ; Jessica D. CRAWFORD, Auteur ; Emma P. ANDERSON, Auteur ; Tiffani CARRASCO, Auteur ; Shimin ZHENG, Auteur ; Gregory A. ORDWAY, Auteur ; Michelle J. CHANDLEY, Auteur . - p.870-884.
Langues : Anglais (eng)
in Autism Research > 13-6 (June 2020) . - p.870-884
Mots-clés : autism cytokines neuroinflammation pathology postmortem white matter Index. décimale : PER Périodiques Résumé : Evidence for putative pathophysiological mechanisms of autism spectrum disorder (ASD), including peripheral inflammation, blood-brain barrier disruption, white matter alterations, and abnormal synaptic overgrowth, indicate a possible involvement of neuroinflammation in the disorder. Neuroinflammation plays a role in the development and maintenance of the dendritic spines involved in glutamatergic and GABAergic neurotransmission, and also influences blood-brain permeability. Cytokines released from microglia can impact the length, location or organization of dendritic spines on excitatory and inhibitory cells as well as recruit and impact glial cell function around the neurons. In this study, gene expression levels of anti- and pro-inflammatory signaling molecules, as well as oligodendrocyte and astrocyte marker proteins, were measured in both gray and white matter tissue in the anterior cingulate cortex from ASD and age-matched typically developing (TD) control brain donors, ranging from ages 4 to 37?years. Expression levels of the pro-inflammatory gene, HLA-DR, were significantly reduced in gray matter and expression levels of the anti-inflammatory gene MRC1 were significantly elevated in white matter from ASD donors as compared to TD donors, but neither retained statistical significance after correction for multiple comparisons. Modest trends toward differences in expression levels were also observed for the pro-inflammatory (CD68, IL1?) and anti-inflammatory genes (IGF1, IGF1R) comparing ASD donors to TD donors. The direction of gene expression changes comparing ASD to TD donors did not reveal consistent findings implicating an elevated pro- or anti-inflammatory state in ASD. However, altered expression of pro- and anti-inflammatory gene expression indicates some involvement of neuroinflammation in ASD. Autism Res 2020, 13: 870-884. © 2020 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: The anterior cingulate cortex is an integral brain region in modulating social behaviors including nonverbal communication. The study found that inflammatory gene expression levels were altered in this brain region. We hypothesize that the inflammatory changes in this area could impact neuronal function. The finding has future implications in using these molecular markers to identify potential environmental exposures and distinct cell differences in autism. En ligne : http://dx.doi.org/10.1002/aur.2284 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427 A pilot open-label trial of minocycline in patients with autism and regressive features / Carlos A. PARDO in Journal of Neurodevelopmental Disorders, 5-1 (December 2013)
[article]
Titre : A pilot open-label trial of minocycline in patients with autism and regressive features Type de document : Texte imprimé et/ou numérique Auteurs : Carlos A. PARDO, Auteur ; A. BUCKLEY, Auteur ; A. THURM, Auteur ; L. C. LEE, Auteur ; A. AZHAGIRI, Auteur ; D. M. NEVILLE, Auteur ; Susan E. SWEDO, Auteur Article en page(s) : p.9 Langues : Anglais (eng) Mots-clés : Autism Bdnf Chemokines Clinical trial Cytokines Metalloproteinases Microglia Minocycline Neuroinflammation Neurotrophins Index. décimale : PER Périodiques Résumé : BACKGROUND: Minocycline is a tetracycline derivative that readily crosses the blood brain barrier and appears to have beneficial effects on neuroinflammation, microglial activation and neuroprotection in a variety of neurological disorders. Both microglial activation and neuroinflammation have been reported to be associated with autism. The study was designed to evaluate the effects of minocycline treatment on markers of neuroinflammation and autism symptomatology in children with autism and a history of developmental regression. METHODS: Eleven children were enrolled in an open-label trial of six months of minocycline (1.4 mg/kg). Ten children completed the trial. Behavioral measures were collected and cerebrospinal fluid (CSF), serum and plasma were obtained before and at the end of minocycline treatment and were analyzed for markers of neuroinflammation. RESULTS: Clinical improvements were negligible. The laboratory assays demonstrated significant changes in the expression profile of the truncated form of brain derived neurotrophic factor (BDNF) (P = 0.042) and hepatic growth factor (HGF) (P = 0.028) in CSF. In serum, the ratio of the truncated BDNF form and alpha-2 macroglobulin (alpha-2 M), was also significantly lower (P = 0.028) while the mature BDNF/alpha-2 M ratio revealed no difference following treatment. Only the chemokine CXCL8 (IL-8) was significantly different (P = 0.047) in serum while no significant changes were observed in CSF or serum in chemokines such as CCL2 (MCP-1) or cytokines such as TNF-alpha, CD40L, IL-6, IFN-gamma and IL-1beta when pre- and post-treatment levels of these proteins were compared. No significant pre- and post-treatment changes were seen in the profiles of plasma metalloproteinases, putative targets of the effects of minocycline. CONCLUSIONS: Changes in the pre- and post-treatment profiles of BDNF in CSF and blood, HGF in CSF and CXCL8 (IL-8) in serum, suggest that minocycline may have effects in the CNS by modulating the production of neurotrophic growth factors. However, in this small group of children, no clinical improvements were observed during or after the six months of minocycline administration. TRIAL REGISTRATION: NCT00409747. En ligne : http://dx.doi.org/10.1186/1866-1955-5-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=345
in Journal of Neurodevelopmental Disorders > 5-1 (December 2013) . - p.9[article] A pilot open-label trial of minocycline in patients with autism and regressive features [Texte imprimé et/ou numérique] / Carlos A. PARDO, Auteur ; A. BUCKLEY, Auteur ; A. THURM, Auteur ; L. C. LEE, Auteur ; A. AZHAGIRI, Auteur ; D. M. NEVILLE, Auteur ; Susan E. SWEDO, Auteur . - p.9.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 5-1 (December 2013) . - p.9
Mots-clés : Autism Bdnf Chemokines Clinical trial Cytokines Metalloproteinases Microglia Minocycline Neuroinflammation Neurotrophins Index. décimale : PER Périodiques Résumé : BACKGROUND: Minocycline is a tetracycline derivative that readily crosses the blood brain barrier and appears to have beneficial effects on neuroinflammation, microglial activation and neuroprotection in a variety of neurological disorders. Both microglial activation and neuroinflammation have been reported to be associated with autism. The study was designed to evaluate the effects of minocycline treatment on markers of neuroinflammation and autism symptomatology in children with autism and a history of developmental regression. METHODS: Eleven children were enrolled in an open-label trial of six months of minocycline (1.4 mg/kg). Ten children completed the trial. Behavioral measures were collected and cerebrospinal fluid (CSF), serum and plasma were obtained before and at the end of minocycline treatment and were analyzed for markers of neuroinflammation. RESULTS: Clinical improvements were negligible. The laboratory assays demonstrated significant changes in the expression profile of the truncated form of brain derived neurotrophic factor (BDNF) (P = 0.042) and hepatic growth factor (HGF) (P = 0.028) in CSF. In serum, the ratio of the truncated BDNF form and alpha-2 macroglobulin (alpha-2 M), was also significantly lower (P = 0.028) while the mature BDNF/alpha-2 M ratio revealed no difference following treatment. Only the chemokine CXCL8 (IL-8) was significantly different (P = 0.047) in serum while no significant changes were observed in CSF or serum in chemokines such as CCL2 (MCP-1) or cytokines such as TNF-alpha, CD40L, IL-6, IFN-gamma and IL-1beta when pre- and post-treatment levels of these proteins were compared. No significant pre- and post-treatment changes were seen in the profiles of plasma metalloproteinases, putative targets of the effects of minocycline. CONCLUSIONS: Changes in the pre- and post-treatment profiles of BDNF in CSF and blood, HGF in CSF and CXCL8 (IL-8) in serum, suggest that minocycline may have effects in the CNS by modulating the production of neurotrophic growth factors. However, in this small group of children, no clinical improvements were observed during or after the six months of minocycline administration. TRIAL REGISTRATION: NCT00409747. En ligne : http://dx.doi.org/10.1186/1866-1955-5-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=345 Tumor necrosis factor-? expression aberration of M1/M2 macrophages in adult high-functioning autism spectrum disorder / T. YAMAUCHI in Autism Research, 14-11 (November 2021)
[article]
Titre : Tumor necrosis factor-? expression aberration of M1/M2 macrophages in adult high-functioning autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : T. YAMAUCHI, Auteur ; M. MAKINODAN, Auteur ; M. TORITSUKA, Auteur ; K. OKUMURA, Auteur ; Y. KAYASHIMA, Auteur ; R. ISHIDA, Auteur ; N. KISHIMOTO, Auteur ; M. TAKAHASHI, Auteur ; T. KOMORI, Auteur ; Y. YAMAGUCHI, Auteur ; R. TAKADA, Auteur ; K. YAMAMURO, Auteur ; S. KIMOTO, Auteur ; Y. YASUDA, Auteur ; R. HASHIMOTO, Auteur ; T. KISHIMOTO, Auteur Article en page(s) : p.2330-2341 Langues : Anglais (eng) Mots-clés : Adult Autism Spectrum Disorder Cytokines Humans Macrophages Monocytes Tumor Necrosis Factor-alpha Tnf-? diagnosis inflammation macrophage monocyte Index. décimale : PER Périodiques Résumé : The etiology of autism spectrum disorder (ASD) is complex, and its pathobiology is characterized by enhanced inflammatory activities; however, the precise pathobiology and underlying causes of ASD remain unclear. This study was performed to identify inflammatory indicators useful for diagnosing ASD. The mRNA expression of cytokines, including tumor necrosis factor-? (TNF-?), was measured in cultured M1 and M2 macrophages from patients with ASD (n = 29) and typically developed (TD) individuals (n = 30). Additionally, TNF-? expression in the monocytes of patients with ASD (n = 7), showing aberrations in TNF-? expression in M1/M2 macrophages and TD individuals (n = 6), was measured. TNF-? expression in M1 macrophages and the TNF-? expression ratio in M1/M2 macrophages were markedly higher in patients with ASD than in TD individuals; however, this increase was not observed in M2 macrophages (M1: sensitivity = 34.5%, specificity = 96.7%, area under the curve = 0.74, positive likelihood ratio = 10.34; ratio of M1/M2: sensitivity = 55.2%, specificity = 96.7%, area under the curve = 0.79, positive likelihood ratio = 16.55). Additionally, TNF-? expression in monocytes did not significantly differ between patients with ASD and TD individuals. In conclusion, further studies on TNF-? expression in cultured macrophages may improve the understanding of ASD pathobiology. LAY SUMMARY: TNF-? expression in differentiated M1 macrophages and TNF-? expression ratio in differentiated M1/M2 macrophages were markedly higher in patients with ASD than in TD individuals, while no difference in TNF-? expression was found in pre-differentiation cells such as monocytes. These measurements allow elucidation of the novel pathobiology of ASD and can contribute to biomarker implementation for the diagnosis of adult high-functioning ASD. En ligne : http://dx.doi.org/10.1002/aur.2585 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450
in Autism Research > 14-11 (November 2021) . - p.2330-2341[article] Tumor necrosis factor-? expression aberration of M1/M2 macrophages in adult high-functioning autism spectrum disorder [Texte imprimé et/ou numérique] / T. YAMAUCHI, Auteur ; M. MAKINODAN, Auteur ; M. TORITSUKA, Auteur ; K. OKUMURA, Auteur ; Y. KAYASHIMA, Auteur ; R. ISHIDA, Auteur ; N. KISHIMOTO, Auteur ; M. TAKAHASHI, Auteur ; T. KOMORI, Auteur ; Y. YAMAGUCHI, Auteur ; R. TAKADA, Auteur ; K. YAMAMURO, Auteur ; S. KIMOTO, Auteur ; Y. YASUDA, Auteur ; R. HASHIMOTO, Auteur ; T. KISHIMOTO, Auteur . - p.2330-2341.
Langues : Anglais (eng)
in Autism Research > 14-11 (November 2021) . - p.2330-2341
Mots-clés : Adult Autism Spectrum Disorder Cytokines Humans Macrophages Monocytes Tumor Necrosis Factor-alpha Tnf-? diagnosis inflammation macrophage monocyte Index. décimale : PER Périodiques Résumé : The etiology of autism spectrum disorder (ASD) is complex, and its pathobiology is characterized by enhanced inflammatory activities; however, the precise pathobiology and underlying causes of ASD remain unclear. This study was performed to identify inflammatory indicators useful for diagnosing ASD. The mRNA expression of cytokines, including tumor necrosis factor-? (TNF-?), was measured in cultured M1 and M2 macrophages from patients with ASD (n = 29) and typically developed (TD) individuals (n = 30). Additionally, TNF-? expression in the monocytes of patients with ASD (n = 7), showing aberrations in TNF-? expression in M1/M2 macrophages and TD individuals (n = 6), was measured. TNF-? expression in M1 macrophages and the TNF-? expression ratio in M1/M2 macrophages were markedly higher in patients with ASD than in TD individuals; however, this increase was not observed in M2 macrophages (M1: sensitivity = 34.5%, specificity = 96.7%, area under the curve = 0.74, positive likelihood ratio = 10.34; ratio of M1/M2: sensitivity = 55.2%, specificity = 96.7%, area under the curve = 0.79, positive likelihood ratio = 16.55). Additionally, TNF-? expression in monocytes did not significantly differ between patients with ASD and TD individuals. In conclusion, further studies on TNF-? expression in cultured macrophages may improve the understanding of ASD pathobiology. LAY SUMMARY: TNF-? expression in differentiated M1 macrophages and TNF-? expression ratio in differentiated M1/M2 macrophages were markedly higher in patients with ASD than in TD individuals, while no difference in TNF-? expression was found in pre-differentiation cells such as monocytes. These measurements allow elucidation of the novel pathobiology of ASD and can contribute to biomarker implementation for the diagnosis of adult high-functioning ASD. En ligne : http://dx.doi.org/10.1002/aur.2585 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450 Cord and Early Childhood Plasma Adiponectin Levels and Autism Risk: A Prospective Birth Cohort Study / R. RAGHAVAN in Journal of Autism and Developmental Disorders, 49-1 (January 2019)
PermalinkMaternal Mid-Gestation Cytokine Dysregulation in Mothers of Children with Autism Spectrum Disorder / S. CASEY in Journal of Autism and Developmental Disorders, 52-9 (September 2022)
PermalinkA pilot dose finding study of pioglitazone in autistic children / L. CAPANO in Molecular Autism, 9 (2018)
PermalinkTH1/Treg ratio may be a marker of autism in children with immune dysfunction / Zu-Qing NIE in Research in Autism Spectrum Disorders, 101 (March 2023)
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