15 results on '"Khajavi, Leila"'
Search Results
2. MeCP2-E1 isoform is a dynamically expressed, weakly DNA-bound protein with different protein and DNA interactions compared to MeCP2-E2
- Author
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Martínez de Paz, Alexia, Khajavi, Leila, Martin, Hélène, Claveria-Gimeno, Rafael, Tom Dieck, Susanne, Cheema, Manjinder S., Sanchez-Mut, Jose V., Moksa, Malgorzata M., Carles, Annaick, Brodie, Nick I., Sheikh, Taimoor I., Freeman, Melissa E., Petrotchenko, Evgeniy V., Borchers, Christoph H., Schuman, Erin M., Zytnicki, Matthias, Velazquez-Campoy, Adrian, Abian, Olga, Hirst, Martin, Esteller, Manel, Vincent, John B., Malnou, Cécile E., and Ausió, Juan
- Published
- 2019
- Full Text
- View/download PDF
3. Influenza vaccination induces autoimmunity against orexinergic neurons in a mouse model for narcolepsy
- Author
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Bernard-Valnet, Raphaël, primary, Frieser, David, additional, Nguyen, Xuan Hung, additional, Khajavi, Leila, additional, Quériault, Clémence, additional, Arthaud, Sébastien, additional, Melzi, Silvia, additional, Fusade-Boyer, Maxime, additional, Masson, Frederick, additional, Zytnicki, Matthias, additional, Saoudi, Abdelhadi, additional, Dauvilliers, Yves, additional, Peyron, Christelle, additional, Bauer, Jan, additional, and Liblau, Roland S, additional
- Published
- 2022
- Full Text
- View/download PDF
4. Tissue-resident CD8+T cells drive compartmentalized and chronic autoimmune damage against CNS neurons
- Author
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Frieser, David, primary, Pignata, Aurora, additional, Khajavi, Leila, additional, Shlesinger, Danielle, additional, Gonzalez-Fierro, Carmen, additional, Nguyen, Xuan-Hung, additional, Yermanos, Alexander, additional, Merkler, Doron, additional, Höftberger, Romana, additional, Desestret, Virginie, additional, Mair, Katharina M., additional, Bauer, Jan, additional, Masson, Frederick, additional, and Liblau, Roland S., additional
- Published
- 2022
- Full Text
- View/download PDF
5. Profilage transcriptionnel des lymphocytes T pathogènes dans la narcolepsie de type I
- Author
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Khajavi, Leila and Khajavi, Leila
- Abstract
La narcolepsie est un trouble du sommeil chronique, à vie, rare et grave résultant de la destruction exclusive et étendue des neurones hypothalamiques produisant le neuropeptide orexine (hypocrétine), entraînant une somnolence diurne excessive (SDE), un sommeil nocturne fragmenté ainsi qu'une cataplexie (paralysie temporaire des muscles volontaires). La prévalence de la narcolepsie en Europe et en Amérique du Nord est d'environ un individu sur deux mille. La narcolepsie affecte à peu près les mêmes proportions chez les hommes et les femmes. Les signes précurseurs apparaissent à la petite enfance ou l'adolescence avec une incidence plus élevée de développement de troubles émotionnels (dépression), cognitifs (problèmes d'attention) et métaboliques (obésité) au fil du temps. Son association à certains déclencheurs environnementaux (exposition saisonnière à des agents pathogènes), la susceptibilité génétique (forte association avec l'antigène leucocytaire humain), le récepteur des cellules T et d'autres loci immunitaires impliquent un processus immunopathologique conduisant à la perte de neurones producteurs d'orexine. Plusieurs études portant à la fois sur des modèles animaux et sur des échantillons humains ont été publiées dans lesquelles les cellules T pathogènes sont supposées être les principaux contributeurs à la destruction sélective et à la dérégulation des neurones producteurs d'orexine dans l'hypothalamus. Ici, nous étudions plus en détail la théorie à médiation auto-immune en comparant le transcriptome de sous-ensembles fonctionnels de cellules T CD4 et CD8 (naïf, effecteur, mémoire effecteure, mémoire centrale) isolés des cellules mononucléées du sang périphérique de patients atteints de narcolepsie ainsi que de donneurs sains et personnes souffrant d'autres troubles du sommeil. Notre objectif est de déterminer les contributions spécifiques de chaque compartiment et sous-ensemble de cellules T au développement de la narcolepsie., Narcolepsy is a chronic, life-long, rare and severe sleep disorder arising as a consequence of the exclusive and extensive destruction of hypothalamic neurons producing the neuropeptide orexin (hypocretin), resulting in excessive daytime sleepiness (EDS), fragmented nocturnal sleep as well as cataplexy (temporary paralysis of voluntary muscles). The prevalence of narcolepsy in Europe and North America is approximately one in two thousand individuals. Narcolepsy affects males and females at roughly the same ratio. Onset occurs in early childhood or adolescence with a higher incidence of the development of emotional (depression), cognitive (attention problems), and metabolic (obesity) disturbances over time. Its association with certain environmental triggers (seasonal pathogen exposure), genetic susceptibility (strong association with the human leukocyte antigen), T-cell receptor and other immune loci implicate an immuno-pathological process leading to the loss of orexin- producing neurons. Several studies in both animal models as well as human samples have been published in which pathogenic T-cells are hypothesized to be the main culprits contributing to the selective destruction and dysregulation of orexin-producing neurons in the hypothalamus. Here, we investigate the autoimmune-mediated theory further by comparing the transcriptome of functional CD4 and CD8 T-cell subsets (naive, effector, effector memory, central memory) isolated from the peripheral blood mononuclear cells of narcolepsy patients as well as healthy donors and individuals suffering from other sleep disorders. Our aim is to determine the specific contributions of each T-cell compartment and subset to the development of narcolepsy.
- Published
- 2021
6. Tissue-resident CD8+ T cells drive compartmentalized and chronic autoimmune damage against CNS neurons.
- Author
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Frieser, David, Pignata, Aurora, Khajavi, Leila, Shlesinger, Danielle, Gonzalez-Fierro, Carmen, Nguyen, Xuan-Hung, Yermanos, Alexander, Merkler, Doron, Höftberger, Romana, Desestret, Virginie, Mair, Katharina M., Bauer, Jan, Masson, Frederick, and Liblau, Roland S.
- Subjects
T cells ,CENTRAL nervous system diseases ,AUTOIMMUNE diseases ,IMMUNOLOGIC memory ,NEURONS ,BLOOD-brain barrier - Abstract
The mechanisms underlying the chronicity of autoimmune diseases of the central nervous system (CNS) are largely unknown. In particular, it is unclear whether tissue-resident memory T cells (T
RM ) contribute to lesion pathogenesis during chronic CNS autoimmunity. Here, we observed that a high frequency of brain-infiltrating CD8+ T cells exhibit a TRM -like phenotype in human autoimmune encephalitis. Using mouse models of neuronal autoimmunity and a combination of T single-cell transcriptomics, high-dimensional flow cytometry, and histopathology, we found that pathogenic CD8+ T cells behind the blood-brain barrier adopt a characteristic TRM differentiation program, and we revealed their phenotypic and functional heterogeneity. In the diseased CNS, autoreactive tissue-resident CD8+ T cells sustained focal neuroinflammation and progressive loss of neurons, independently of recirculating CD8+ T cells. Consistently, a large fraction of autoreactive tissue-resident CD8+ T cells exhibited proliferative potential as well as proinflammatory and cytotoxic properties. Persistence of tissue-resident CD8+ T cells in the CNS and their functional output, but not their initial differentiation, were crucially dependent on CD4+ T cells. Collectively, our results point to tissue-resident CD8+ T cells as essential drivers of chronic CNS autoimmunity and suggest that therapies targeting this compartmentalized autoreactive T cell subset might be effective for treating CNS autoimmune diseases. A local contribution to CNS autoimmunity: Aberrantly activated tissue-resident memory T cells (TRM ) have been shown to contribute to inflammatory conditions. Their role in the CNS remains unclear. Now, in two complementary studies, Vincenti et al. and Frieser et al. investigated the role of TRM in the CNS. Vincenti and colleagues reported that after viral brain infection, TRM triggered CNS inflammation, promoting autoimmune reactions in mice. Cells with TRM -like phenotype were also identified in brain tissue from patients with CNS autoimmune diseases. Frieser et al. used rodent models of CNS autoimmunity to show that pathogenic CD8+ T cells infiltrating the CNS adopted a TRM phenotype that contribute to the disease. The results suggest that targeting TRM can be effective in treating CNS autoimmune diseases. [ABSTRACT FROM AUTHOR]- Published
- 2022
- Full Text
- View/download PDF
7. Dietary antioxidants and fibre intake and depressive symptoms in Iranian adolescent girls
- Author
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Khayyatzadeh, Sayyed Saeid, primary, Omranzadeh, Alireza, additional, Miri-Moghaddam, Mohammad Mobin, additional, Arekhi, Soheil, additional, Naseri, Amirhosein, additional, Ziaee, Amirhosein, additional, Khajavi, Leila, additional, Nejati Salehkhani, Fatemeh, additional, Ferns, Gordon A, additional, and Ghayour-Mobarhan, Majid, additional
- Published
- 2020
- Full Text
- View/download PDF
8. Dietary antioxidants and fibre intake and depressive symptoms in Iranian adolescent girls.
- Author
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Khayyatzadeh, Sayyed Saeid, Omranzadeh, Alireza, Miri-Moghaddam, Mohammad Mobin, Arekhi, Soheil, Naseri, Amirhosein, Ziaee, Amirhosein, Khajavi, Leila, Nejati Salehkhani, Fatemeh, Ferns, Gordon A, and Ghayour-Mobarhan, Majid
- Subjects
TEENAGE girls ,IRANIANS ,MENTAL depression ,FOOD consumption ,VITAMIN C ,DIETARY fiber ,TEENAGERS - Abstract
Objective: To investigate the cross-sectional association between dietary intakes of antioxidants and fibre and depressive symptoms among Iranian adolescent girls. Design: A cross-sectional population-based study. Setting: Primary schools in two different cities located in northeastern Iran (Mashhad and Sabzevar). Participants: A total of 988 adolescent girls aged 12–18 years were included in the study. Results: Subjects with no or minimal depression symptoms had significantly higher dietary intakes of α-carotene (P = 0·01), β-carotene (P = 0·006), lutein (P = 0·03) and vitamin C (P = 0·04) when compared with subjects with mild-to-severe depression symptoms. Soluble dietary fibre and insoluble dietary fibre intakes were also significantly higher in healthy adolescents compared with those with depression symptoms (P < 0·001). In multivariate-adjusted model 2, the OR (95 % CI) of depressive symptoms were 0·61 (95 % CI 0·37, 1·01), 0·42 (95 % CI 0·26, 0·69), 0·50 (95 % CI 0·31, 0·79), 0·71 (95 % CI 0·44, 1·15), 0·51 (95 % CI 0·32, 0·82) and 0·42 (95 % CI 0·25, 0·68) for the highest v. lowest quartile of vitamin C, β-carotene, α-carotene, lutein, soluble dietary fibre and insoluble dietary fibre cereal intakes, respectively. Conclusions: Dietary intake of some antioxidants and dietary fibre intake was inversely associated with depression symptoms among Iranian adolescent girls. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
9. MeCP2-E1 isoform is a dynamically expressed, weakly DNA-bound protein with diferent protein and DNA interactions compared to MeCP2-E2
- Author
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Canadian Institutes of Health Research, Genome British Columbia, University of Victoria, McGill University, Max Planck Society, German Research Foundation, European Commission, Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, Ministerio de Educación, Cultura y Deporte (España), Canadian Cancer Society Research Institute, Fundación la Caixa, Generalitat de Catalunya, Calcul en Midi-Pyrénées, Centro Nacional de Investigaciones Oncológicas (España), SCOAP, Ausió, Juan [0000-0002-9674-6717], Martínez de Paz, Alexia, Khajavi, Leila, Martin, Hélène, Claveria-Gimeno, Rafael, Dieck, S. T., Cheema, Manjinder S., Sánchez-Mut, José V., Moksa, Malgorzata M., Carles, Annaick, Brodie, Nick I., Sheikh, Taimoor I., Freenan, Melissa E., Petrotchenko, Evgeniy V., Borchers, Christoph H., Schuman, Erin M., Zytnicki, Matthias, Velázquez-Campoy, Adrián, Abian, Olga, Hirst, Martin, Estelller, Manel, Vincent, John B., Malnou, Cécile E., Ausió, Juan, Canadian Institutes of Health Research, Genome British Columbia, University of Victoria, McGill University, Max Planck Society, German Research Foundation, European Commission, Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, Ministerio de Educación, Cultura y Deporte (España), Canadian Cancer Society Research Institute, Fundación la Caixa, Generalitat de Catalunya, Calcul en Midi-Pyrénées, Centro Nacional de Investigaciones Oncológicas (España), SCOAP, Ausió, Juan [0000-0002-9674-6717], Martínez de Paz, Alexia, Khajavi, Leila, Martin, Hélène, Claveria-Gimeno, Rafael, Dieck, S. T., Cheema, Manjinder S., Sánchez-Mut, José V., Moksa, Malgorzata M., Carles, Annaick, Brodie, Nick I., Sheikh, Taimoor I., Freenan, Melissa E., Petrotchenko, Evgeniy V., Borchers, Christoph H., Schuman, Erin M., Zytnicki, Matthias, Velázquez-Campoy, Adrián, Abian, Olga, Hirst, Martin, Estelller, Manel, Vincent, John B., Malnou, Cécile E., and Ausió, Juan
- Abstract
BACKGROUND: MeCP2-a chromatin-binding protein associated with Rett syndrome-has two main isoforms, MeCP2-E1 and MeCP2-E2, differing in a few N-terminal amino acid residues. Previous studies have shown brain region-specific expression of these isoforms which, in addition to their different cellular localization and differential expression during brain development, suggest that they may also have non-overlapping molecular mechanisms. However, differential functions of MeCP2-E1 and E2 remain largely unexplored. RESULTS: Here, we show that the N-terminal domains (NTD) of MeCP2-E1 and E2 modulate the ability of the methyl-binding domain (MBD) to interact with DNA as well as influencing the turn-over rates, binding dynamics, response to neuronal depolarization, and circadian oscillations of the two isoforms. Our proteomics data indicate that both isoforms exhibit unique interacting protein partners. Moreover, genome-wide analysis using ChIP-seq provide evidence for a shared as well as a specific regulation of different sets of genes. CONCLUSIONS: Our study supports the idea that Rett syndrome might arise from simultaneous impairment of cellular processes involving non-overlapping functions of MECP2 isoforms. For instance, MeCP2-E1 mutations might impact stimuli-dependent chromatin regulation, while MeCP2-E2 mutations could result in aberrant ribosomal expression. Overall, our findings provide insight into the functional complexity of MeCP2 by dissecting differential aspects of its two isoforms.
- Published
- 2019
10. La narcolepsie de type 1 est-elle d’origine auto-immune ?
- Author
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Chabod, Marianne, primary, Khajavi, Leila, additional, and Liblau, Roland S., additional
- Published
- 2019
- Full Text
- View/download PDF
11. A variant in CYP2R1 predicts circulating vitamin D levels after supplementation with high‐dose of vitamin D in healthy adolescent girls
- Author
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Khayyatzadeh, Sayyed Saeid, primary, Mehramiz, Mehrane, additional, Esmaeily, Habibollah, additional, Mirmousavi, Seyed Jamal, additional, Khajavi, Leila, additional, Salehkhani, Fatemeh Nejati, additional, Hanachi, Parichehr, additional, Bahrami‐Taghanaki, Hamidreza, additional, Eslami, Saeed, additional, Vatanparast, Hasan, additional, Ferns, Gordon A., additional, Avan, Amir, additional, and Ghayour‐Mobarhan, Majid, additional
- Published
- 2019
- Full Text
- View/download PDF
12. MeCP2-E1 isoform is a dynamically expressed, weakly DNA-bound protein with different protein and DNA interactions compared to MeCP2-E2
- Author
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de Paz, Alexia Martínez, primary, Khajavi, Leila, additional, Martin, Hélène, additional, Claveria-Gimeno, Rafael, additional, Dieck, Susanne tom, additional, Cheema, Manjinder S., additional, Sanchez-Mut, Jose V., additional, Moksa, Malgorzata M., additional, Carles, Annaick, additional, Brodie, Nick I., additional, Sheikh, Taimoor I., additional, Freeman, Melissa E., additional, Petrotchenko, Evgeniy V., additional, Borchers, Christoph H., additional, Schuman, Erin M., additional, Zytnicki, Matthias, additional, Velazquez-Campoy, Adrian, additional, Abian, Olga, additional, Hirst, Martin, additional, Esteller, Manel, additional, Vincent, John B., additional, Malnou, Cécile E., additional, and Ausió, Juan, additional
- Published
- 2018
- Full Text
- View/download PDF
13. Association of dysglycemia with mortality in children receiving parenteral nutrition in pediatric intensive care unit
- Author
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Khajavi, Leila, primary, Khademi, Gholamreza, additional, Mehramiz, Mehraneh, additional, Norouzy, Abdolreza, additional, and Safarian, Mohammad, additional
- Published
- 2018
- Full Text
- View/download PDF
14. Tissue-resident CD8 + T cells drive compartmentalized and chronic autoimmune damage against CNS neurons.
- Author
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Frieser D, Pignata A, Khajavi L, Shlesinger D, Gonzalez-Fierro C, Nguyen XH, Yermanos A, Merkler D, Höftberger R, Desestret V, Mair KM, Bauer J, Masson F, and Liblau RS
- Subjects
- Animals, Central Nervous System, Immunologic Memory, Mice, Neurons, Autoimmune Diseases pathology, CD8-Positive T-Lymphocytes
- Abstract
The mechanisms underlying the chronicity of autoimmune diseases of the central nervous system (CNS) are largely unknown. In particular, it is unclear whether tissue-resident memory T cells (T
RM ) contribute to lesion pathogenesis during chronic CNS autoimmunity. Here, we observed that a high frequency of brain-infiltrating CD8+ T cells exhibit a TRM -like phenotype in human autoimmune encephalitis. Using mouse models of neuronal autoimmunity and a combination of T single-cell transcriptomics, high-dimensional flow cytometry, and histopathology, we found that pathogenic CD8+ T cells behind the blood-brain barrier adopt a characteristic TRM differentiation program, and we revealed their phenotypic and functional heterogeneity. In the diseased CNS, autoreactive tissue-resident CD8+ T cells sustained focal neuroinflammation and progressive loss of neurons, independently of recirculating CD8+ T cells. Consistently, a large fraction of autoreactive tissue-resident CD8+ T cells exhibited proliferative potential as well as proinflammatory and cytotoxic properties. Persistence of tissue-resident CD8+ T cells in the CNS and their functional output, but not their initial differentiation, were crucially dependent on CD4+ T cells. Collectively, our results point to tissue-resident CD8+ T cells as essential drivers of chronic CNS autoimmunity and suggest that therapies targeting this compartmentalized autoreactive T cell subset might be effective for treating CNS autoimmune diseases.- Published
- 2022
- Full Text
- View/download PDF
15. [An autoimmune basis for narcolepsy type 1?]
- Author
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Chabod M, Khajavi L, and Liblau RS
- Subjects
- Autoimmune Diseases epidemiology, CD4-Positive T-Lymphocytes physiology, Case-Control Studies, Genetic Association Studies, Genetic Predisposition to Disease, HLA-DQ beta-Chains genetics, Humans, Immune System physiology, Narcolepsy epidemiology, Narcolepsy immunology, Orexins physiology, Autoimmune Diseases complications, Autoimmunity physiology, Narcolepsy etiology
- Published
- 2019
- Full Text
- View/download PDF
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