Proteomic and Metabolomic Characterization of COVID-19 Patient Sera

Cell, Journal Year: 2020, Volume and Issue: 182(1), P. 59 - 72.e15

Published: May 28, 2020

Language: Английский

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Rethinking IL-6 and CRP: Why they are more than inflammatory biomarkers, and why it matters

Brain Behavior and Immunity, Journal Year: 2018, Volume and Issue: 70, P. 61 - 75

Published: March 1, 2018

Language: Английский

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Systemic lupus erythematosus: Diagnosis and clinical management

Journal of Autoimmunity, Journal Year: 2018, Volume and Issue: 96, P. 1 - 13

Published: Nov. 16, 2018

Language: Английский

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Therapeutic Mechanisms of Glucocorticoids

Trends in Endocrinology and Metabolism, Journal Year: 2017, Volume and Issue: 29(1), P. 42 - 54

Published: Nov. 20, 2017

Language: Английский

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Therapeutic strategies for COVID-19: progress and lessons learned

Nature Reviews Drug Discovery, Journal Year: 2023, Volume and Issue: 22(6), P. 449 - 475

Published: April 19, 2023

Language: Английский

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Inflammation in psychiatric disorders: what comes first?

Annals of the New York Academy of Sciences, Journal Year: 2018, Volume and Issue: 1437(1), P. 57 - 67

Published: May 11, 2018

Abstract Neuropsychiatric disorders (i.e., mood and schizophrenia) inflammation are closely intertwined, possibly powering each other in a bidirectional loop. Depression facilitates inflammatory reactions promotes depression neuropsychiatric disorders. Patients with exhibit all cardinal features of inflammation, including increased circulating levels inducers, activated sensors, mediators targeting tissues. Inflammation may contribute to the pathophysiology clinical progression these Of note, proinflammatory cytokines modulate behavior cognition by reducing brain monoamine levels, activating neuroendocrine responses, promoting excitotoxicity (increased glutamate levels), impairing plasticity. What sources this chronic inflammation? Increasing evidence indicates that changes regulation, metabolism, diet/microbiota, negative health behaviors important triggers inflammation. Finally, recent data indicate early‐life stress is associated overt prior development

Language: Английский

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Tuberculosis: progress and advances in development of new drugs, treatment regimens, and host-directed therapies

The Lancet Infectious Diseases, Journal Year: 2018, Volume and Issue: 18(7), P. e183 - e198

Published: March 23, 2018

Language: Английский

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Discriminating mild from critical COVID-19 by innate and adaptive immune single-cell profiling of bronchoalveolar lavages

Cell Research, Journal Year: 2021, Volume and Issue: 31(3), P. 272 - 290

Published: Jan. 21, 2021

Abstract How the innate and adaptive host immune system miscommunicate to worsen COVID-19 immunopathology has not been fully elucidated. Here, we perform single-cell deep-immune profiling of bronchoalveolar lavage (BAL) samples from 5 patients with mild 26 critical in comparison BALs non-COVID-19 pneumonia normal lung. We use pseudotime inference build T-cell monocyte-to-macrophage trajectories model gene expression changes along them. In COVID-19, CD8 + resident-memory (T RM ) CD4 T-helper-17 H17 cells undergo active (presumably antigen-driven) expansion towards end trajectory, are characterized by good effector functions, while they remain more naïve. Vice versa, T-cells T-helper-1 characteristics H1 -like) expressing exhaustion markers EX enriched halfway their where also exhibit show evidence inflammation-associated stress at trajectories. Monocyte-to-macrophage that chronic hyperinflammatory monocytes alveolar macrophages, otherwise anti-inflammatory antigen-presenting characteristics, depleted. contribute an ATP-purinergic signaling-inflammasome footprint could enable associated fibrosis disease-severity. Finally, viral RNA-tracking reveals infected lung epithelial cells, a significant proportion neutrophils macrophages involved clearance.

Language: Английский

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Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation

Frontiers in Psychiatry, Journal Year: 2019, Volume and Issue: 10

Published: March 11, 2019

Early life stressors display a high universal prevalence and constitute major public health problem. Prolonged psychoneurobiological alterations as sequelae of early stress (ELS) could represent developmental risk factor mediate for disease, leading to higher physical mental morbidity rates in later life. ELS exert programming effect on sensitive neuronal brain networks related the response during critical periods development thus lead enduring hyper- or hypo-activation system altered glucocorticoid signaling. In addition, emotional autonomic reactivity, circadian rhythm disruption, functional structural changes brain, well immune metabolic dysregulation have been lately identified important factors chronically impaired homeostatic balance after ELS. Furthermore, human genetic background epigenetic modifications through stress-related gene expression interact with these explain inter-individual variation vulnerability resilience stress. This narrative review presents relevant evidence from mainly research ten most acknowledged neurobiological allostatic pathways exerting adverse effects even decades (hypothalamic-pituitary-adrenal axis, nervous system, inflammation, oxidative stress, cardiovascular gut microbiome, sleep genetics, epigenetics, structural, correlates). Although findings back causal relation between psychobiological maladjustment life, precise trajectories their temporal coincidence has not elucidated yet. Future studies should prospectively investigate putative mediators sequence, while considering potentially delayed time-frame phenotypical expression. Better screening strategies are needed better individual prevention treatment.

Language: Английский

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Tumors induce de novo steroid biosynthesis in T cells to evade immunity

Nature Communications, Journal Year: 2020, Volume and Issue: 11(1)

Published: July 17, 2020

Abstract Tumors subvert immune cell function to evade responses, yet the complex mechanisms driving evasion remain poorly understood. Here we show that tumors induce de novo steroidogenesis in T lymphocytes anti-tumor immunity. Using a transgenic steroidogenesis-reporter mouse line identify and characterize steroidogenic cells, defining global gene expression identity of these steroid-producing cells regulatory networks by using single-cell transcriptomics. Genetic ablation restricts primary tumor growth metastatic dissemination models. Steroidogenic dysregulate immunity, inhibition pathway is sufficient restore This study demonstrates as mechanism immunosuppression potential druggable target.

Language: Английский

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